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Research Projects: Mutations in the Mstn Gene Essay

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Updated: Feb 28th, 2022

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.

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