Category: Gene

Introduction: The Miracle of Genetics. Defining Epigenetics

The problems of genetics have always been drawing people’s attention. No matter what level technological development people can reach, the idea of entering the genetic domain still seems rather creepy and at the same time very promising. Hence the weird attraction and awe towards identical twins (Araniel, 2012) and other paradoxes of genetics comes.

However, having an identical, or enzygotic twin means sharing not only every single feature, but also a range of genetic diseases. However, with the help of epigenetics, the above-mentioned problem can be solved. Defined as the study of changes within a human body that have been enhanced by other factors than genetic ones, epigenetics can help avoid genetic diseases that run in the family.

A Different Perspective on Epigenetics: Article Discussion

Found in the Genomics & Genetics Weekly journal, the article titled New epigenetics study results reported from M.D. Anderson Cancer Center allows for a better understanding of the genetic mechanisms in developing leukemia. According to the research hypothesis, with the help of epigenetics, a more detailed analysis of the factors enhancing myeloid leukemia is possible.

To be more exact, the increase of DNA methylation, which decreases the risk of developing leukemia, is possible to achieve by converting 5-methyl-cytosine to 5-hydroxymethyl-cytosine enzymatically with the help of TET2 (New epigenetics study results reported from M.D. Anderson Cancer Center, 2013). According to the research results, “Thus, TET2 mutations affect global methylation in CMML but most of the changes are likely to be outside gene promoters” (New epigenetics study results reported from M.D. Anderson Cancer Center, 2013).

The strong points of the research: concerning the innovations

It must be admitted that the research makes efficient use of the newest technologies. Moreover, it is essential that the researchers studied “chronic myelomonocytic leukemia (CMML) samples” (New epigenetics study results reported from M.D. Anderson Cancer Center, 2013), thus, offering a solution to the diseases that used to be a death sentence.

The scope of research and other limitations: questioning the credibility

However, it is also necessary to point out that the research conducted by New epigenetics study results reported from M.D. Anderson Cancer Center also has its limitations. Among the most obvious ones, the scope of the research should be mentioned. Since only 30 people took part in the research, it is not yet possible to assume that a panacea for genetic diseases has been discovered.

Concerning the major findings: the role of the gene promoters

The research shows that genetically, a predisposition to a certain type of illness can be modified, once a certain outer factor is introduced into the organism. Moreover, the research shows that the intervention is highly likely to be successful: “total 5-methyl-cytosine levels in TET2 mutant cases were significantly higher than TET2 wild-type cases (median=14.0% and 9.8%, respectively) (p=0.016” (New epigenetics study results reported from M.D. Anderson Cancer Center, 2013).

Family History Worksheet Analysis: When Genealogy and Genetics Go Hand in Hand

Weirdly enough, being predisposed to a specific disease does not mean necessarily having to face them in the future. Knowing the problem means winning half the battle; therefore, a careful study of the family genealogy must be conducted.

Feeling safe: what does not seem to be the problem

The two obvious issues to take into account are diabetes and cancer. However, of all the possible problems, the two above-mentioned seem the least possible. The test shows that only distant relatives have the diabetes; moreover, one of the instances had a childhood onset, which means that the symptoms of diabetes are unlikely to develop at present.

Checking the threat department: where the danger lurks

However, certain issues might appear rather problematic. According to the test results, the parents suffer from allergies and asthma. On the one hand, the latter could have developed due to unhealthy lifestyle led after the birth of a child and, therefore, have no impact on the latter.

On the other hand, the test shows that the sibling is also asthmatic. Hence, it can be considered that asthma is also among the possible threats In addition, such issue as allergies is worth a serious consideration. Since the parents are allergic to certain elements, it is necessary to check what exactly causes allergy in parents and be extremely careful with the rest of possible allergens (Family history worksheet, n. d.).

Preventing the storm: the possible steps to be undertaken

Speaking of asthma, breathing exercises and specific medicine can be prescribed to prevent the outbreaks of the disease. As for allergies, keeping far away from the possible allergens is required; however, it is also needed to run several tests to determine the exact allergens that trigger the reaction.

Vitality Coach Recommendations: Worksheet Two Analysis

As it has been mentioned, the diseases that run in the family had been considered inevitable for any family member up to the point at which the epigenetics postulates have been formulated. Considering genetic diseases will help develop the strategy to avoid these illnesses in the future.

Dieting issues: something fishy

There is no need to stress the significance of dieting any harder; it is obvious that good nutrition rules help improve the organism clockwork and prevent a number of diseases from happening. According to the results that the worksheet has provided, it is crucial to choose vegetables, fruit and fish as the basis for diet.

Exercises and physical activity

However, even with the most well balanced diet, getting into shape is hardly possible unless one takes up the right exercises. As the test results how, with the help of physical activity, some of the genetic issues with weight gain and anxiety can be resolved. Moreover, the test results say that daily exercises will help having a good sleep at night (Worksheet 2. Vitality coach recommendations, n. d.).

Getting a grip: emotions control

According to the results of the completed questionnaire, there are also certain emotional issues that need to be addressed. According to the research data, anxiety, sleep deprivation and communicational problems do not come from a genetic background, but are a result of stressful life and the inability to control emotions. Therefore, it will be necessary to reconsider my lifestyle and start working on my emotions control, which will help fight my predisposition to the above-mentioned diseases.

Conclusion: There Is Yet Much to Learn. Epigenetics Takes off

Judging by the potential that epigenetics has nowadays, and the opportunities that it opens for the studies in genetics, there is a whole new world of discoveries ahead. While there is yet much to learn, it is clear even now that with the help of epigenetics, the cure for a number of genetic diseases can be found.

Reference List

Family history worksheet (n. d.). PDF file. 22 March 2013.

New epigenetics study results reported from M.D. Anderson Cancer Center (2013). Genomics & Genetics Weekly, 95. Web.

Araniel (2012). NOVA scienceNOW: 33 – epigenetics. Retrieved from https://www.youtube.com/watch?v=xG8nt9OlODo

Worksheet 2. Vitality coach recommendations (n. d.) MS Word file. 22 March 2013.

Neural Stem Cells

The nervous system is comprised of specialized type of cells called Neural Stem Cells (NSCs). These cells undergo differentiation and proliferation resulting to a mass of undifferentiated cells. This progeny then undergoes differentiation into the many cells of the nervous system. From neural stem cells, cell of central nervous system such as astrocytes, neurons, ependymal cells and oligodendrocytes are formed.

Developmental versatility of plasticity of neural stem cells is important in formation of these different neural cells. A NSC can either be embryonic stem cell of adult stem cell. Embryonic stem cells are fully versatile and can form any cell type. On the other hand, adult stem cells have no versatility to form any cell type but replace multipotent cells when they wear out or die. In this regard, embryonic stem cells can either be totipotent, pluripotent or multipotent.

Totipotent stem cells are the most potent cells and can therefore give rise to any type of body cell. Pluripotent stem cells can give rise to body tissues but lack full potency to give rise to any cell type. Multipotent stem cells are the least plastic cells and can only form certain cell types.

Neural cell division (neurogenesis) is an important process in brain development but it needs to be regulated during adulthood development. The best understood neural cell differentiation pathways are sparked by growth factors. Certain set of growth factors are optimal for development of certain stages of neural stem cells. For instance, fibroblast growth factors (FGF) are selective for development of early neural stem cells. This means that in absence of FGF, there occurs a significant reduction in the number stem cell divisions.

For the purposes of studies, multipotent stem cells can be isolated from brain tissue or embryonic stem cells. This can be achieved through co-culture of embryonic stem cells in stroma or conditioned medium. These cells can then be preserved for use in studies together with other cell type-models. These cells and models have enhanced the understanding of the processes involved during brain development.

Stem cell isolation from embryonic cells in central nervous system and in periphery nervous system is achieved through direct means. A neural puncture is usually made and the cells cultured in medium. Apart from stem cell isolation from brain, other regions (hippocampus and ventricular zone) can be used during isolation of adult stem cell.

Viral Vectors in Gene Therapy

Gene therapy refers to a medical application of genetics where genetic transformations are utilized in therapeutic functions. This field has objectively transformed medical fields especially in treatment of chronic disease which are hard to cure by use of chemotherapy e.g. cancer.

This exercise requires transfer of target genes into target cells of the patient. In so doing, a transfer agent called a vector is important. Viruses have lately been found useful as vectors. A good example of a virus that has been used in gene therapy is Adenovirus. It has been found out that this genus of viruses have a good profile to transfer target genes to target cell. They have been used substantially in cancer gene therapy and in biomedicine.

Replication-defective adenovirus has extensively been used as a vector to transfer transgenes to targeted cancerous cells and tumors. On the other hand, oncolytic adenoviruses which have capacity to replicate have been used to kill or transfer therapeutic genes to infected target cells.

Viral vectors have been developed through altering the viral genome making its expression impossible. For instance alteration of E1A gene of Adenovirus genome led to a replication-defective strain. E1A gene is important in ensuring that viral genome is expressed and therefore it can induce its multiplication of host cell. Replication-competent adenoviruses are made by integrating a therapeutic gene in their genome.

Restriction Enzymes

Restriction enzymes are an important part in many genetic applications. They enable genome excision by recognizing specific recognition sites along a genetic strand. Excision is important as it allows formation of recombinant genetic strands. A major source of restriction enzymes is bacteria.

Bearing in mind that bacterial genetic material has similar properties to any other genetic material; one may wonder why their DNA remains intact in presence of restriction enzymes. This is possible because restriction enzymes have a way of differentiating between self DNA and non-self DNA. This is possible because Bacterial DNA has other groups attached to their nucleotide sequences. These may be methyl group and/or carbohydrates.

Restriction enzymes were discovered way back in 1952. Their mode of functioning was however not well known until 1960 when Wemer Arber presented his findings with the help of Dussoix at the First International Biophysics Congress. Their research was accompanied by two theories that there was an enzyme in host bacterial cell that cuts its DNA at specific sequences and that host DNA was unaffected due to the presence of methylase. The research earned them the Plantamour-Prevost prize.

Restriction enzyme was first isolated in Escherichia coli by Meselson and Yuan. The enzyme was essentially seen to offer protection of the DNA from the viral DNA which would infect the cells.

Gene therapy conducted through human gene transfer is an experimental techniqe applied for curing some genetic and inherited illnesses. The technics yet provided no clear and reliable results since the first clinical experiment was held in 1990 (Sheridan 122), but still it is widely applied on the experimental basics (Richards 2). There are many debates on the question of gene transfer from the ethical point of view. In this paper, the principles of Plato’s justice will be applied to discuss human gene transfer.

Gene therapy is a process of transferring of genetic material that is DNA or RNA into individual’s body. The technique:

“is being studied to see whether it could treat certain health problems by either compensating for defective genes, prompting the body to make a potentially therapeutic substance, or triggering the immune system to fight disease” (“National Institutions of Health” par. 1).

Gene therapy also known as human gene transfer is applied for treatment of such diseases as myeloma, leukemia, hemophilia, Parkinson disease and some other diseases of genetic or inherited nature. The major principle of the approach is inserting a virus with a modified gene into a patient’s body in hope that the virus while in-building its genome into patient’s cells will provide a cell with a capability to produce normal proteins or the proteins that will provide a cure for the targeted disease.

Thus, the technique is majorly experimental, not providing clear results many debates are raised on this question. Some speculate that human genetic transfer can be applied as a gene doping for athletes (Kayser, Mauron, and Miah 2). There are also many questions raised by the perspective of gene modification conducted to a fetus or a child on parent’s request in attempts to provide with some features that are unlikely to be inherited in a natural way. Some claims of the ethical basis are that a child has a right to be born as it is without any additional improvements (Powell 57). Human genetic transfer theoretically can be applied into a healthy adult individual for improving such functions as memory, metabolism, mental and physical capabilities.

These debates highly correlate with Plato’s views on philosophy of justice. Plato’s understanding of justice was that “Justice is not the right of the stronger but the effective harmony of the whole” (Bhandari par.18), meaning that everything should be in its natural places; performing the function assigned by the Universe or the general order (Plato’s State) will collapse. Another definition of justice lies within specialization, meaning that everyone should perform their own duties, not the duties of another person. In case of genetic therapy, this statement can be applied dually. On one hand, if not treated from a fatal disease the organism will die or will function improperly thus the inner harmony will be ruined and injustice will take place.

Therefore, treatment will be justified. On other hand, if applied to the healthy organism, the genetic therapy will provide it with the capabilities, not provided by nature, thus shifting its specialization to the sphere not assigned to it initially. This would be unfair according to Plato’s theory. Plato’s idea of non-interference also can be applied to the first example of genetic treatment that individuals with an illness have their own specialization, thus treatment should not be provided as a disease is something assigned by the nature. This is if to look from the global point of view.

In general, the application of Plato’s concept of justice gives the idea that the practice of human genetic transfer is unfair, but still there are some issues that might stand for its justice.

Works Cited

Bhandari, Durai R. Plato’s Concept Of Justice: An Analysis. n.d. Web.

Kayser, Bengt, Alexandre Mauron, and Andy Miah. “Current Anti-doping Policy: a Critical Appraisal.” BMC Medical Ethics 8.1 (2007): 2. BioMed Central. Web.

National Institutions of Health: NIH Backgrounder on Gene Transfer 2004. Web.

Powell, Russell, and Allen Buchanan. “Breaking Evolution’s Chains: The Prospect of Deliberate Genetic Modification in Humans.” Journal of Medicine and Philosophy 30.1 (2011): 57-59. Print.

Richards, Sabrina. “Gene Therapy Arrives in Europe.” The Scientist 1.1 (2012): 2. Print.

Sheridan, Cormac. “Gene Therapy Finds Its Niche.” Nature Biotechnology 29.2 (2011): 121-128. Print.

Background

Caenorhabditis elegans is a nonparasitic, translucent roundworm that is commonly found in temperate soil ecosystems (Husson et al., 2009). Its length is approximately 1 millimeter even though adult worms can grow to a length of 1.5 millimeters. The worm is unsegmented and has a pseudocoelom. It does not have a respiratory and a circulatory system. The gut of C. elegans contains gut pellets that emanate a bright blue fluorescence, which is predominant when the animal dies. Most of these roundworms are hermaphrodites. However, the male worms possess dedicated tails for mating, which have spicules.

C. elegans is an extensively investigated experimental prototypical organism that has led to great discoveries in the field of genetic analysis. Some of the features that contribute to its applicability in genetic studies include a short, three-day life cycle, small size, and an uncomplicated laboratory cultivation process (Andersen, Krichevsky, Leheste, & Moloney, 2008). Hundreds of these roundworms can be cultivated on one Petri dish containing a lawn of Escherichia coli as the source of food. In addition, the worm has been used to study molecular biology techniques such as RNA interference. Also, the worm is often used as a model to study physiological processes that occur in higher organisms (Benian & Epstein, 2011).

The unc-22 gene codes for the production of a protein called twitchin, which is a gigantic intracellular protein with numerous fibronectin- and immunoglobulin-like realms. The protein also contains one protein kinase domain that resembles titin. The unc-22 gene is fundamental in tissues where it controls the actinomyosin contraction-relaxation cycle. The gene is also responsible for the sustenance of standard muscle morphology. Unc-22 interacts with the muscle protein myosin and is confined to A-bands of the worm’s striated muscles that make up the wall of the animal’s body. The unc-22 proteins can add phosphate groups to the light chain peptides that make up myosin and go through autophosphorylation outside a living organism. Twitchin influences muscle synchronization in C. elegans and controls muscular contraction. Interference with the unc-22 gene in C. elegans affects its function leading to compromised movement and the characteristic “twitcher” phenotype.

Studies involving the manipulation of the unc-22 gene including the introduction of mutations and silencing various alleles of the gene have helped elucidate the structure and function of the gene, which is beneficial to the field of muscle physiology.

Research Question

Which alleles of the unc-22 gene elicit the strongest response in muscle movement when mutated?

The unc-22 gene is fascinating because of its rare phenotype. Distorted alleles of the locus bring about different degrees of compromised movement and muscle incompetence. Weak alleles show a minimal effect on the motion or organization of the muscle. When strong alleles are affected, the result is almost complete paralysis of adult worms. Moreover, there may be aberrant muscle structure where the thick and thin filaments are available in the usual amounts, but their distribution is altered. However, all alleles result in a continuous, subcellular jerk in all the cells making up the muscles of the body wall. It has been reported that the alleles of the unc-54 myosin heavy-chain gene and one of lev-ll alleles also contribute to this observation further indicating the interaction of unc-22 with other alleles. The twitch is aggravated by choline agonists.

Hypothesis

If the strong alleles of the unc-22 gene are knocked down, the strongest muscle movement will be evident.

Specific Aims

To test for the interference of the strong alleles of the unc-22 gene, different alleles of the unc-22 genes will be introduced with mutations and the strength of the mutations on muscle function will be evaluated.

Genetic investigations have provided a number of intuitions about the nature of the gene and its function. The unc-22 gene is an abnormally large mutational target such that the intragenic recombination rates for alleles at the far ends of the gene are equal or higher than rates observed for the most secluded allelic pairs of the unc-54 gene that encodes the myosin heavy chain. Most alleles of the unc-22 gene are conditionally dominant. Therefore, animals with heterozygous mutations in the unc-22 gene exhibit normal motion as well as conventional muscle structure. Nevertheless, they can be provoked to jerk forcefully in solutions containing choline agonists. This dominance implies that the unc-22 gene most likely encodes a protein that is needed stoichiometrically to exert its effects. An interesting observation is that the reversion analysis of unc-22 alleles shows that specific missense alleles of the myosin heavy-chain gene unc-54 can overpower the unc-22 phenotype. Several changes occur from this procedure including repression of the muscle twitch, partial restitution of motility and reorganization of the muscle structure. Sequence evaluation of the unc-54 repressors reveals that the transmutations are present in the region that encodes the myosin head, a few are situated around the nucleotide binding domain while others are located close to the preserved thiol domain.

The 1^st Specific Aim: Forward genetic screen

A study by Chu et al. (2014) has shown that the “twitcher” phenotype can be provoked by putting worms without the unc-22 gene on 1% nicotine resulting in violent twitching by the mutant worms for several hours. The wild-type worms become rigid and restrained. Nicotinic agonists such as levamisole can also be used for this test. Therefore, placing the worms on 1% nicotine solution will enable the screening of mutant worms from the wild-type worms by observing the twitching thus visually separating the mutant worms from the wild-type worms.

The 2^nd Specific Aim: Reverse genetic screen of mutation

Muscular twitching is a consequence of defective unc-22 gene. A deletion of the unc-22 gene should produce abnormal muscle twitching in C. elegans. Unc-22 RNAi will be introduced to the worm and observe the resultant phenotypes. Thereafter, the gene loci responsible for the mutation will be isolated and mapped. The unc-22 gene has multiple loci and alleles, and only a few of these loci will produce the twitching phenotype. It is reported that the large protein is responsible for muscular contraction because this protein is often found localized to the Actin A of myosin. Therefore, the absence of this protein in the isolated loci will indicate the particular loci that are greatly affected by this mutation.

The 3^rd Specific Aim: To determine strong and weak unc-22 alleles

To determine the alleles that lead to strong phenotypes of unc-22, a mutation analysis will be done by placing Tc1 insertions in the unc-22 region. The first step will be isolating genomic DNA from the wild-type and extracting the unc-22 regions. Approximately 12 different Tc1 insertions will then be placed into a minimum of 10 different sites in the unc-22 alleles, which have already been identified (Thompson et al., 2013). These recombinant fragments will then be used to transform different C. elegans samples using E. coli cloning vectors. The process of transformation will be relatively simple because C. elegans feeds on E. coli. The ingested bacteria cells containing the mutant alleles will then be incorporated into the host cell genome leading to the manifestation of the unc-22 phenotype. The transformed animals will be labeled accordingly based on the specific allele that was mutated. The impact of the insertions in the phenotype will be determined by observing the movement of the animals in the presence and the absence of choline inhibitors. The strength of the muscular twitching will be scored to determine which mutations have the strongest impact on the muscular contraction of C. elegans. Minimal twitching will be indicative of weak unc-22 alleles while aggressive and prolonged twitching will show strong unc-22 alleles.

Research Objectives

Broader Impact

Understanding the mutation of the unc-22 genes and the particular alleles that lead to strong muscle impairment will improve the understanding of structure and muscle function. The unc-22 gene is similar to the TTN and OBSCN genes in humans that function in muscle contraction (Matsunaga, Qadota, Furukawa, Choe, & Benian, 2015). TTN gene codes for a large predominant protein of the striated muscle. Mutations in this gene are linked to human diseases such as familial hypertrophic cardiomyopathy 9, hereditary myopathy and muscular dystrophy. Also, patients with the autoimmune disease scleroderma have been reported to produce antibodies against titin.

The obscurin gene is responsible for the production of a protein that belongs to the category of colossal sarcomeric signaling proteins such as titin and nebulin. It may play a significant role in the arrangement of myofibrils in the course of assembly and may facilitate associations between the sarcoplasmic reticulum and myofibrils. The obscurin gene is thought to take part in various physiological processes such as apoptosis, initiation of programmed cell death via extracellular indications, cell differentiation, the development of multicellular organisms, the addition of phosphate groups to amino acids in proteins and the control of Rho protein signal transduction.

Knowledge of the strongest mutations can help in the development of appropriate gene therapies to remedy the illnesses caused by the mutation of these genes.

Future Directions

Following the identification of the strong alleles in unc-22 mutations, future studies could look into ways of protecting against these mutations.

References

Andersen, J., Krichevsky, A., Leheste, J. R., & Moloney, D. J. (2008). Caenorhabditis elegans as an undergraduate educational tool for teaching RNAi. Biochemistry and Molecular Biology Education, 36(6), 417-427.

Benian, G. M., & Epstein, H. F. (2011). Caenorhabditis elegans muscle: A genetic and molecular model for protein interactions in the heart. Circulation Research, 109(9), 1082-1095.

Chu, J. S. C., Chua, S. Y., Wong, K., Davison, A. M., Johnsen, R., Baillie, D. L., & Rose, A. M. (2014). High-throughput capturing and characterization of mutations in essential genes of Caenorhabditis elegans. BMC Genomics, 15(1), 361.

Husson, S. J., Landuyt, B., Nys, T., Baggerman, G., Boonen, K., Clynen, E.,… & Schoofs, L. (2009). Comparative peptidomics of Caenorhabditis elegans versus C. briggsae by LC–MALDI-TOF MS. Peptides, 30(3), 449-457.

Matsunaga, Y., Qadota, H., Furukawa, M., Choe, H. H., & Benian, G. M. (2015). Twitchin kinase interacts with MAPKAP kinase 2 in Caenorhabditis elegans striated muscle. Molecular Biology of the Cell, 26(11), 2096-2111.

Thompson, O., Edgley, M., Strasbourger, P., Flibotte, S., Ewing, B., Adair, R.,… & Kieffer, A. (2013). The million mutation project: A new approach to genetics in Caenorhabditis elegans. Genome Research, 23(10), 1749-1762.

CRISPR: A Powerful New Way to Edit DNA

What exactly is CRISPR?

CRISPR (clustered regularly interspaced short palindromic repeats) is an exclusive molecular system, which aims to change the structure of genes and exclude potentially dangerous cells that can adversely affect a particular organism. By adding to a DNA chain, this system can edit some sectors and remove from them those genes that are harmful. Similarly, CRISPR fights against bacteria and viruses that enter the human body.

In what ways could humans apply this new technology for practical purposes?

According to scientists, the effect of this molecular system on the example of a man has not yet been investigated to the end. However, there are already some positive results: many dairy producers note the effectiveness of CRISPR in combating bacterial cultures that are contained in yogurts and cheese against harmful viruses (Pollack par.15). Moreover, scientists managed to conduct successful experiments on monkeys by changing their genes (Pollack par. 6)

How is CRISPR different from other gene-editing technologies?

Unlike some other technologies that change the structure of DNA, CRISPR completely disables a particular gene and does not just partially edit it (Pollack par. 32). The potential of this system is quite significant because it may help to change the chain of information embedded in a body even at the stage of development. CRISPR allows completely getting rid of a particular gene and convert it as required.

Summary of the Article

The article “A Powerful New Way to Edit DNA” by Andrew Pollack tells about a new innovative molecular system called CRISPR, its capabilities, and its applications. Scientists working on its creation conducted a series of experiments on living organisms and got a rather unexpected and certainly significant result. CRISPR proved that it could fight with various pathogenic viruses and completely change the chains of DNA, thereby preventing harmful and mutational changes. So far, no experiments on humans have been conducted. Nevertheless, scientists suppose that they will be able to prove the effectiveness of this system in treating various mutations and genetic changes at the embryo stage shortly enough (Pollack par. 7).

As for the pros, there are several positive aspects that the introduction of CRISPR can bring into medicine. First, as Pollack notes, it is a rather practical step from a commercial point of view (par. 12). Various food producers, as well as farmers, are ready to use this technology to preserve the quality of their products and prevent premature spoilage. Perhaps, such use of CRISPR will not be available to everyone but only to the most advanced companies since this system is unlikely to be cheap. Secondly, this method of genetic change substantially accelerates the process of work on rearranging a DNA chain. If earlier scientists needed a lot of time, now, according to Pollack, this procedure can be done in one step (par. 28). Probably, this feature of the system is one of the most evident and undeniable advantages.

However, the system has its cons. For example, CRISPR raises ethical issues (Pollack par. 10). Despite the success of experiments on animals, the introduction of the system into a human body can cause unforeseen consequences. Furthermore, a change in what is inherent to nature is perhaps too bold a step. Also, according to the author, a possible problem is the delivery of a necessary structure for those cells that need to be changed (Pollack 39). In case of failure, the outcome of such an experiment will be unforeseen. Thus, CRISPR is a rather controversial technology regarding the need for its use, but the fact of an innovative discovery that can change the world and nature of a person is significant and undeniable. The wealthiest people will likely be able to experience the impact of this system since its cost will certainly be high. Judging by the results, the humanity will gain access to CRISPR soon enough, and the whole world is watching how this program is being developed and when its visible results will appear.

Work Cited

Pollack, Andrew. “A Powerful New Way to Edit DNA.”The New York Times, 2014, Web.

Introduction

The expansion of poly-glutamines present in the Huntingtin proteins is solely responsible for the Huntington disease. The Huntington disease refers to a dominant autosomal neurodegenerative aberration. To understand the development of the Huntington disease, the function of normal Huntingtin proteins has to be elucidated. This is accomplished by purifying the Huntingtin proteins and Argonaute as associated proteins.

Studies have shown that Huntingtin proteins and Argo2 exist in P bodies and that a decline in Huntingtin led to a compromised RNA-mediated gene silencing. RNA-mediated gene silencing refers to the related processes that involve 21 to 25 nucleotide RNAs to repress the expression of specific target genes.

A change in the Huntingtin protein leads to a distinct neurodegeneration pattern. This paper, therefore, seeks to establish whether the Huntington disease protein is a contributory factor in RNA- mediated gene silencing. The paper is based on a research study titled Huntington’s disease protein contributes to RNA-mediated gene silencing through association with Argonaute and P bodies by Savas et al. (2008).

With regard to this, the paper seeks to test the hypothesis that Huntingtin protein causes a characteristic neurodegeneration pattern. This hypothesis is informed by a study on mouse striatal cells with mutant Htt that reveals the presence of fewer P bodies and a decreased gene silencing activity. This may suggest that transcriptional deregulation in Huntington disease is an outcome of the mutant Htt’s role post-transcriptional processes.

In order to test the hypothesis, Savas et al used a biochemical approach to purify proteins related to WT and mutant Htt and identified Ago2 as a co-purifying protein (Savas et al., p. 10820). Further co-localization tests showed the presence of Htt and Ago2 in processing P bodies, cytoplasmic foci that contain translationally repressed mRNAs with bound proteins (Savas et al., p. 10820).

The data suggested that normal Htt is a component of the P body and functions in the ost-transcriptional pathways (Savas et al., p. 10820). The results of the test indicate that Ago2 indeed co-purifies with Huntingtin. Specifically, Ago2 co-purifies with Htt 480 protein when over-expressed in cells.

The test further proved that Huntingtin is present in P bodies (Savas et al., p. 10822). It was also established that Huntingtin plays a role in small RNA- mediated processes (Savas et al., p. 10823). Finally, a comparison was made between normal Huntingtin and polyQ-expanded Huntingtin (Savas et al., p. 10824). The findings of this research may help in control and management of Huntington disease.

Background

The background of this research is based on RNA silencing, which refers to the process of sequence-specific regulation of gene expressions caused by double-stranded RNA (Fire et al, p. 806). It takes place in almost all eukaryotes. Some of the functions of the RNA silencing remain largely controversial while a few are well documented. RNA silencing processes mediate transcriptional and post-transcriptional gene silencing. Post-transcriptional gene silencing is characterized by mRNA degradation or translational repression.

Extensive complementarity between the double-stranded RNA and RNA is required for effective target mRNA degradation. However, imperfect complementarity may also produce effective translational repression, but without extensive target RNA degradation (Olsen & Ambros, p. 671). RNA silencing is a crucial process in both plants and animals as it allows for the regulation of development and the control of transposition events. It also plays an anti-viral role in plants and in insects such as Drosophila melanogaster (Voinnet, p. 206).

The processing of double-stranded RNA and siRNA requires the ribonuclease (RNase) 3 Dicer. After the RNA generation, one of the siRNA strands is incorporated into a complex with a constituent of the Argonaute protein family. The complex is then allowed to cleave or repress translation.

Scholars have attempted to describe the characterization of a new RNA polymerase that is responsible for the gene silencing. One such scholar is David Balaucombe who was able to identify the sd4 mutant, which was ineffective in the siRNA production and methylation of a retro-element, and which also indicated a partial loss of trans-gene silencing. Balaucombe’s studies revealed that plants encode subunits for a fourth polymerase in addition to the common DNA-dependent RNA polymerases 1, 2 and 3.

Mutational studies show that polymerases are able to silence certain transposons and repetitive DNA involving RNA-dependent RNA polymerase Rdr2 and RNase 3 Dcl3. This possibly explains why chromatin silencing depends on RNA transcription. In addition, Pol 4 may be resistant to DNA or chromatin modifications that impact on polymerases 1, 2 and 3 and, therefore, is able to maintain the silenced state.

Preliminary Results

Savas et al conducted their experiment to test the hypothesis that Huntingtin protein causes a characteristic neurodegeneration pattern. Preliminary results posted a number of findings. First and foremost, it was concluded that Ago2 co-purifies with Huntingtin.

This was informed by a discovery-based Htt purification plan, which was aimed at identifying the interactions and differences between proteins that co-purify with WT and mutant Htt.

In the experiment, HeLa cells were used to create stable cell lines that express Flag-tagged Htt N-terminal 590 aa with 25 or 97 glutamines (Flag-Htt 590-25Q or Flag-Htt 590-97Q) (Savas et al., p.10820). A cytoplasmic S100 fraction was prepared from these cells and subjected to immune-purification with Flag-M2 agarose followed by peptide elution (Savas et al., p.10820).

HeLa cells are purposely used because they provide large materials that help in identification of interacting proteins. During the test, SDS/PAGE was used to isolate the peptide eluted fraction, which was then stained with coomassie blue (Savas et al., p.10820). This produced the right molecular weight of Flag-Htt590 and a limited number of nonstoichiometric co-purifying proteins.

The gel lanes were then partitioned and subjected to in-gel tryptic digestion, which was followed by ESI-MS/MS based peptide sequencing (Savas et al., p.10820). Many of the distinct co-purifying polypeptides corresponded with the Argonaute proteins. This confirmed that the Ago family of proteins is responsible for small RNA gene-mediated silencing (Peters and Meister, p. 611).

Proteins associated with Ago2 from HEK293T were purified separately and 40 unique peptides corresponding to the endogenous Htt was identified (Savas et al., p.10822). This interaction was established by the co-precipitation and immune-blotting. Tests further revealed that Huntingtin is present in P bodies.

This was investigated by the localization of transfected Htt and Ago2 by confocal microscopy (Savas et al., p.10822). This was done by transfecting HeLa cells with Myc-Htt590-25Q and Flag-Ago2 and then examined by indirect immuno-flourescence (Savas et al., p.10822). It was observed that the cells expressing these proteins had distinct foci, indicating strong co-localization of the two proteins (Savas et al., p.10822).

Preliminary results also link Huntington to small RNA-mediated processes (Savas et al., p.10823). This finding was investigated by using a Luc reporter to determine the effect of Htt knockdown on the silencing of the mRNA transcripts (Savas et al., p.10823).

This was accomplished by transfecting HeLa cells with GW182, Htt, or Ago2 siRNA and further co-transfecting them with SV40 promoter-Luc reporter plasmid and siRNA to Luc (Savas et al., p.10823). The results of this experiment indicated that cells transfected with Ago2 siRNA posted a five-time increase in reporter activity (Savas et al., p.10823). This confirms that Huntingtin plays a role in small RNA-mediated processes.

Future experiment proposals

A possible future experiment could involve the isolation of Flag-tagged WT (25Q) and polyQ-expanded (97Q) Htt protein complexes from HeLa cell cytoplasmic S100 fraction. Eluates from immuno-purrified Flag Htt 590 should be resolved by 10% SDS/PAGE and visualized by coomassie blue staining (Savas et al., p.10823). Verification of Ago2 as an Htt590 interactor should be done before probing the presence of antibodies in the Flag immuno-precipitates from the cell lysates.

Cytoplasmic extract from HEK293T cells stably expressing Flag-Ago2 or Flag-vector (Mock) should be immuno-precipitated with α-Flag M2 antibody and probed with α-Htt (HDB4E10, Abcam) or α-Flag antibody. HeLa cells should then be co-transfected with Myc-Htt590–25Q, -97Q or deletion mutant (ΔQ or ΔP) and Flag-Ago2.

Ago2 should be immuno-precipitated with α-Flag antibody and the presence of Htt be determined by immuno-blotting with α-Myc antibody. For the experiment to be more accurate, it important to verify the components of the reactions at each stage. Care should also be taken while extracting and culturing of specimens to be used in the experiments.

The RNA-mediated processes have continued to intrigue the science world. However, in spite of the rapid technological advances, studies and experiments on these processes remain largely rudimentary. Consequently, they present several weaknesses, which future attempts should address. Future experiments should take into account the quality of siRNA used in sequencing, invasive transfection reagents and differences in cell lines and culture conditions (Frantz, p. 763).

Future experiments should also build on the RNAi-dependent chromatin-based silencing pathway that was reported in fission yeast Schizosaccharomyces pombe. This may lead to better methods and guidelines for siRNA sequence selection, which are essential in combating the current setbacks caused by the trial-and-error methods.

In addition, there is need to develop more efficient system of delivery and regulation of tissue-specific expressions of siRNA. Lastly, it is important to develop additional RNAi protocols for genome-wide screens. This will assist in the accurate identification of genes involved in specific biological processes.

This experiment is expected to yield results that further prove that Huntingtin disease protein contributes to RNA-mediated gene silencing through association with Argonaute and P bodies. This is because Huntingtin is present in P bodies and this association is highlighted in these experiments.

Conclusion

The various tests conducted for the purpose of this research have gone a long way in establishing Huntingtin and the RNA-mediated gene silencing through association with Ago2 and P bodies. The tests were able to show that Ago2 co-purifies with Huntingtin, that Huntingtin is Present in P bodies and was able to compare normal and polyQ-expanded Huntingtin.

The findings of this report will hopefully pave the way for new ways of tackling certain gene-mediated complexes. A part from further equipping the world of medicine, it could lead to better plant and animal production as it would be possible to engineer genes to achieve certain qualities in organisms. More research is needed in this area in order to achieve long term success.

Works Cited

Fire, Andrew et al. “Potent and Specific Genetic Interference by Double-Stranded RNA in Caenorhabditis Elegans”. Nature 391 (1998): 806-811. Print.

Frantz, Simon. “Studies Reveal Potential Pitfalls of RNAi.” Nat. Rev. Drug Discovery 2 (2003): 763-764. Web.

Olsen, Philip H. and Ambros, Victor. “The Lin-4regulatory RNA Controls Developmental Timing in Caenorhabditis Elegans by Blocking LIN-14 Protein Synthesis After the Initiation of Translation.” Dev. Biol. 216.2 (1999): 671-680. Web.

Peters, Lasse and Meister, Gunter. “Argonaute Proteins: Mediators of RNA Silencing.” Mol Cell 26 (2007): 611–623. Web.

Savas, Jeffrey N. et al. “Huntington’s Disease Protein Contributes to RNA-mediated Gene Silencing Through Association with Argonaute and P Bodies.” PNAS 105.31 (2008): 10820-10825. Web.

Voinnet, Oliver. “Induction and Suppression of RNA Silencing: Insights from Viral Infections.” Nat. Rev. Genet. 6 (2005): 206-220. Print.

Breeding highly productive cows is a priority task for the modern agricultural sector, which is required to produce large volumes of meat products in a short time. Numerous research projects have been aimed at finding a solution to the problem of optimization, including biological one, of the correlation of time and cost resources. The natural mutation taking place in the gene responsible for the protein Myostatin has become an excellent solution to initiate intensive growth of muscle fibers without developing adipose tissue. Thus, from a consumer’s point of view, suppressing the Myostatin gene’s activity allows obtaining a fat-free meat product.

Normally, a healthy body contains the MSTN gene responsible for the biological synthesis of Myostatin protein. According to the karyotypic map, this DNA site is located on the long arm of the second chromosome at 32.2 sites (MSTN myostatin). The protein produced, also known as growth and differentiation factor 8, GDF8, belongs to the family of transforming growth factors of the beta group and performs an inhibitory function for ACVR2B receptors (MSTN Gene). A mutation in this gene leads to impaired protein synthesis and, therefore, to uncontrolled growth of animal muscle tissue.

The nature of this mutation, which leads to disruption of the normal functioning of connective tissue, is the implementation of the gene knockout. It should be noted beforehand that the length of the nucleotide sequence of MSTN is equal to 6627 molecules of nitrogenous bases, and the deletion of 939 and 940 nucleotides — as it was shown for dogs — led to the disturbance of the amino acid sequence of a polypeptide (Mosher et al. 2). As a result of removing two nucleotides, the cysteine amino acid was replaced by a stop codon that interrupted the protein transmission. Consequently, such cows do not have fatty tissue maturation, and this intensifies the growth of muscle fibers.

However, this protein can be controlled or at least inhibited by the synthesis processes of Myostatin in muscle cells. Such methods of destruction can take place on both the molecular level and the genetic one. First of all, it concerns the natural inhibitors of protein activity: Creatine. Creatine is a nitrogen-containing carboxylic acid that inhibits the function of Myostatin by reducing the synthesis of mRNA in molecular chains (Chilibeck et al. 213). In addition, an alternative option for the destruction of this molecule is the elimination of the cholesterol-associated siRNA gene, which leads to a temporary decrease in the concentration of this protein (Khan et al. 1). Targeted removal of a specific nucleotide sequence is possible using genetic manipulation mechanisms known as CRISPR-Cas9 (Zhong et al. 2). It follows that some of the methods suitable for the specific task are appropriate to stimulate the development of muscle fibers.

Identification of a mutation in the MSTN gene can also be implemented by several methods, including molecular dynamics. In particular, the simulation methods can detect modified behavior concerning RMSD and RMSF for two gene permutations, which indirectly indicated modification in the final amino acid sequence (Rasal et al. 3). In addition, sequencing of the body’s genome to determine single-nucleotide polymorphism is the standard mutation method (Dall’Olio et al. 4). This mechanism is based on comparing a given sequence of nitrogenous bases of the long arm of the second chromosome with a reference one, which is typical for this species. Any deviation may indicate a mutation with the potential to disrupt protein synthesis.

Thus, it should be noted that protein Myostatin is a biologically active molecule responsible for the natural suppression of muscle tissue development and differentiation. The fission that occurs with this nucleotide sequence of DNA, located in the long arm of the second cattle chromosome, leads to a violation of protein synthesis and, therefore, to unlimited muscle growth. In cows, this is observed as double muscularity: their meat products have a low-fat content. This mutation can be controlled genetically or molecularly inhibited with creatine. In addition, through the development of genotypic sequencing, researchers can determine the occurrence of mutational processes in the MSTN.

Works Cited

Chilibeck, Philip D., et al. “Effect of Creatine Supplementation During Resistance Training on Lean Tissue Mass and Muscular Strength in Older Adults: A Meta-Analysis.” Open Access Journal of Sports Medicine, vol. 8, 2017, pp. 213-226.

Dall’Olio, Stefania, et al. “Analysis of Horse Myostatin Gene and Identification of Single Nucleotide Polymorphisms in Breeds of Different Morphological Types.” Journal of Biomedicine and Biotechnology, vol. 2010, 1-11.

Khan, Tayeba, et al. “Silencing myostatin using cholesterol-conjugated siRNAs induces muscle growth.” Molecular Therapy-Nucleic Acids, vol. 5, 2016, 1-9.

Mosher, Dana S., et al. “A Mutation in the Myostatin Gene Increases Muscle Mass and Enhances Racing Performance in Heterozygote Dogs.” PLoS Genetics, vol. 3, no.5, 2007, pp. 1-8.

“MSTN Gene.” Medline Plus, 2020. Web.

“MSTN myostatin [ Bos taurus (cattle) ].” NCBI, 2020. Web.

Rasal, Kiran Dashrath, et al. “Identification of Deleterious Mutations in Myostatin Gene of Rohu Carp (Labeo rohita) Using Modeling and Molecular Dynamic Simulation Approaches.” BioMed Research International, vol. 2016, 1-10.

Zhong, Zhaomin, et al. “Targeted Disruption of sp7 and Myostatin with CRISPR-Cas9 Results in Severe Bone Defects and More Muscular Cells in Common Carp.” Scientific Reports, vol. 6, 2016, 1-14.

Germ line gene manipulation (GLGM) is the alteration of genomic content of zygotes or gametes by inserting genes into the Genome of Germ Cells. These alterations affect the genomic content of future generations. With the advent of technology, GLGM is currently performed on infants to alter their germ cells. This procedure is mostly successful if carried out in infants in embryonic stages. GLGM application is used for correcting or preventing genetic deficiencies. What happens is that properly functioning genes are transferred into reproductive cells. GLGM are also used for enhancing genetic cells. This procedure influences traits of the unborn child such as physical appearance or even mental abilities. Successful enhancement of these procedures would be passed to many generations (Carter, 2002, p. 1).

Why should we keep repeating bad genes to our future generation if you can get rid of these diseases once and for all? These questions have been going through parents minds since the invention of germline gene therapy or pre-implantation gene diagnosis. However, before parents decide to undertake the procedure, they should look at the scientific and ethical implications of genetically modified babies before spending all that money in designing their own babies.

Pre-implantation Genetic Diagnosis is a technique that requires the use of test tube baby technique (IVF) to test foetus for genetic disorders before it’s implanted to the uterus. There has been an increase of genetic disorders that can now be easily be prevented through this technique, however, parents should note that not all disorders can be diagnosed in this way. For example, single gene disorder such as cystic fibrosis can be examined under this gene manipulation while genetic disorders such as Duchenne’s muscular dystrophy or hemophilia can only be performed on males. Therefore, when PGD is carried out on the cell is examined to determine the sex of the embryo, only female embryos can be replaced (Marcus, 2004, online). Ethically, PGD increases inequality since only wealthy parents are able to select traits that will guarantee them happiness, creativity and physical talents while families of lower class are left to deal with heart diseases, alcoholism, mental illness and obesity. Also, PGD promotes stigmatisation and discrimination against people with genetic impairments if they could not afford the procedure. Actually, testing could promote a culture of prevention and perfectionism rather than promoting a culture of intolerance (Kersten, 2008, p. 8).

PGD has been reported to misdiagnose as caused by chromosomal mosaicism. For embryos with heterozygous and dominant disorders, mosaicism causes a problem for the PGD of chromosome abnormalities and aneuploidy causing a problem to the foetus. For diagnosis of chromosome abnormalities before PGD is performed is time consuming and technically difficult due to the probe non-availability (Harper et al 2001, p. 11).

Parents should not spend whatever they wish on gene manipulation because if the replacement genes are not correctly inserted into the chromosome may cause a new mutilation in the genome genes permanently impairing the genetic changes that are passed on to the future generations. Another disadvantage of GLGM is that it causes infertility arising from gene manipulation. When unidentified changes are done in the Uterus to the Germ line by gene transfer, the foetus when matures becomes unable to produce off-springs when it grows up. It also requires considerable amount of time to reduce the burden of genetic diseases and this could cause parents a lot of money. Essentially, GMGL is not the most efficient way of eliminating genetic disorders from human gene pool (Carter, 2002, p. 1: Beauchamn & LeRoy, 1999).

Ethically, Germ line gene manipulation is like playing with God. First, individuals should not be let to make decisions about other individuals. Secondly, the power of biotechnology altering God’s handwork is morally wrong. This steams out the debate of the existence or non-existence God. This gene manipulation causes the problem of identity. GMGL changes the identity of the recipient by the act of gene manipulation but person identity is not affected since embryos do not have any memories that need to be altered. It’s morally believed that embryos have moral status that prevent human beings from being genetically tampered with therefore parents should not invest all their savings trying to alter genes that cannot be interfere with. It is required of patients to give informed consent to any medical procedure; therefore this gene manipulation does not give the future generations opportunity to consent to such procedures giving us a moral dilemma for GLGM interventions. GMGL proponents argue that the procedure should be carried out regardless of future generation consent as they do not have rights since they do not exist. They claim that the only right their posses is being born from genetic diseases of which the germ line gene are trying to change (Carter2002, p.1; Gregory & Camplell, 2000).

It is possible that GLGM recipients will not equal access opportunities to employment and insurance. It is argues that some societal institutions will take advantage of this by trying to discriminate against those who have or have not undergone the gene manipulation. These potential institutions include insurance companies, educational institutions, employers and social security. If parents agree to implement GLGM, it will be necessary to implement privacy laws that will prevent exploration of institutions which might take time and money to effect (Carter, 2002, p. 2; Walters & Palmer, 1997).

Canadian researchers in 2005 discovered that attractive children received more attention that ugly ones. More on the reports, a field study was conducted in a supermarket where children entering the store were charged on the attention their get from shop attendants. Their attractiveness was judged on a ten-point scale. On following the children around, the researchers discovered that 1.2 % of homely kids received less attention as compared to the 13.3% of the cutest kids. These findings convey bitter truth, but who determines the cutest scale. How does beauty look like? Is this the reason why parents want to spend all that money in gene manipulation? Actually, beauty is commercialised, what looks cute 10 years ago is not what looks cute today. So, what happens if they change the cute genes today, then 10 years down the line the beauty scales change? Will they take the 10-year grown kid to the doctor and change the genes again? Children should be let to grow up naturally as God intended, decision to determine their beauty should be left to themselves when they grow up. If they decide to do so, they should consider plastic surgery (Green, 2007, p.67).

List of References

1. Beauchamn, L, Tom., & LeRoy W., (eds) 1999, Contemporary Issues in Bioethics, Wadsworth Publishers, California
2. Carter, L. 2002, ‘Germ Line Gene modification. Office of Public Policy and Ethics’, Fact sheet 4, pp. 1-2.
3. Gregory, S., & Campell, J. (eds.) 2000, Engineering the Human Germ Line: An Exploration of the Science and Ethics of altering the Gene We Pass to Our Children’ Oxford University Press, New York
4. Green, M. Ronald. 2007, Babies by design: the of genetic choice, Yale University Press.
5. Harper, C. Joyce, Delhanty, Joy, D. A., & Handyside, Alan, H, 2001, Preimplantation Genetic Diagnosis, John Wiley and Sons.
6. Kersten, E, 2008, The ethical Implication of Preimplantion Genetic Diagnosis (PDG). Web.
7. Marcus, S. 2004, IVF techniques: Pre-implantation Genetic Diagnosis (PGD), IVF-Infertility.com, Web.
8. Walters. L., & Palmer, J. 1997, The ethics of Human Gene Therapy, Oxford University Press, New York.

In the scientific world, gradual body change is a common occurrence witnessed in many parts of the world over a couple of years. The physical changes result from genetic disorders when proteins that play a critical role in the human body are altered. Different gene mutation causes alternately in the sequence of bases in a gene. Examples of gene mutation include chromosomal and point mutation (Lu et al., 2018). A single change in chromosome structure results in physical malfunction. These changes have a devastating effect on the human body and the environment in general.

The genetic alienation of deoxyribonucleic acid (DNA) is altered by exposure to environmental chemicals and mutation. Effects of mutation are either heritable or may only be carried by a single individual (Cocchi et al., 2020). DNA and Ribonucleic acid (RNA) are built by nucleic acid block; hence the presence of harmful chemicals deters the cell’s composition of body organisms (Lu et al., 2018). Somatic mutations result in diseases of the cell, such as cancer that affects vital body organs.

Genetic counselling and testing should be encouraged to parents before having their offspring. Thus, this assists in curbing the adverse effect of contraction of diseases and possible cell disorders of the infant. Testing can be done inform of amniocentesis or chorionic villus sampling (Cocchi et al., 2020). Infants should be screened to make necessary advances to avoid mutation. Moreover, gene therapy is one of the effective methods of treating cancerous infection caused by modification, viral infection, and gene disorder. Furthermore, gene therapy can be done in various ways, including inserting a new gene into the human body to combat disease and substituting a mutated gene. This can be done either outside or inside the body. Cell therapy acts as an earlier treatment in the earlier stages.

In conclusion, the mutation causes a physical dysfunction and change in the complexity of an organism’s body. It is caused by environmental exposure to chemicals or even inherited from parents. Genetic counselling is essential in that it reduces the possibility of mutation. The transformation can cause deletion or even depletion of genes. Thus, this genetic therapy helps administer treatment in the early stages to reduce severe effects.

References

Lu, J., Jin, M., Nguyen, S. H., Mao, L., Li, J., Coin, L. J., Yuan, Z. & Guo, J. (2018). Non-antibiotic antimicrobial triclosan induces multiple antibiotic resistance through genetic mutation. Environment International, 118, 257-265.

Cocchi, E., Nestor, J., & Gharavi, A. (2020). Clinical genetic screening in adult patients with kidney disease. Clinical Journal of the American Society of Nephrology, 15(10), 1497-1510.

The title of this article is the U.S. Companies Announce Plans for Gene-Edited Strawberries. The article explains two companies — Plant Sciences Inc. and J.R. Simplot Company — that want to launch gene-edited strawberries for the first time. An organization that produces genetically modified potatoes has agreed to assist companies in growing strawberries. These strawberries will stay fresh for a longer time and have a longer growing season. The author of this article is Keith Ridler; he is from the associated press and mainly covers breaking news and other news about the environment.

The article explains that growers in the U.S. will produce more than $2.15 billion in strawberries in 2020. According to Keith, one of the problems that farmers encountered, especially in 2020, is that a large percentage of the strawberries produced got spoiled. Therefore, producing genetically modified strawberries will lower such wastes and make the products available to many consumers throughout the year.

Keith further explains that the technology used in the production of potatoes is the same going to be used to produce strawberries. The article records that, currently, there is no proof of whether gene-edited organisms are harmful for human consumption. However, altering the genetic codes of certain foods presents ethical issues. For instance, genetically-modified potatoes have been passed as safe to eat by the U.S. Environmental Protection Agency and U.S. Food and Drug Administration.

For instance, more than 450,000 million kilograms have been sold in 40 states, 4,000 supermarkets; 9,000 restaurants across the country. Keith explains that Cole, the company CEO, has already submitted information to the agricultural department that considers gene modification as a natural process. Hence, there is no need to get regulatory approval before selling products to the market.

The author outlines five types of strawberries that have been developed and perform the best in different climates. The genetic system of these strawberries is complex and adds to their long circle of breeding. Therefore, one needs to look at large populations of seedlings annually to progress with the breeding of traditional plants. Through gene editing, these processes will be done faster because the main goal is to increase their lifespan and enhance their resistance to diseases.

According to Keith Ridler, farmers who will set aside $70,000 for planting and harvesting gene-edited strawberries are likely to lower the risk of crop failure. Simplot is the first agricultural company to be licensed to perform gene modification. These enable scientists to make alterations to the genetic structure of living organisms and have a broad application for enhancing the production of quality plant products.

This article by Keith is relevant to the materials learned in class in that it explains how genes in strawberries have been modified to produce better strawberries that can survive in severe environments and stay for a longer time without getting spoiled. This is relevant to the topic in class about genes, where scientists look forward to modifying the genes of pigs to create organs that can be used as transplants for human beings.

Reading this article has helped me understand that genetic engineering is vital in agriculture. This is because it increases crop production, lowers the cost of food and drug production, and reduces the need for pesticides. In addition, there is improved quality of food and nutrients composition, resistance to diseases and pests, increased food security, and medical advantages to the increasing number of people across the globe. Advancements have been made in creating crops that mature faster; able to survive in harsh conditions such as drought, salt, and frost, as well as other stressors in the environment. This allows them to survive in areas where they would not have flourished.

Works Cited

Ridler, Keith. U.S. Companies Announce Plans for Gene-Edited Strawberries. (2021). Web.