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Meiosis and the Production of Gametes

The process by which a parent cell divides twice, generating four daughter cells, each of which contains half as much genetic information as the parent cell, which signifies that the daughter cells are haploid, is termed meiosis. Meiosis is responsible for the production of gametes in every cycle of cell division. It culminates in the production of four daughter cells (Kallen 2020). The size and shape of the daughter cells are analogous to those of the mother cells, but the chromosome number is different. The daughter cells are haploid. In meiosis, segregation and recombination take place. The process takes place in the reproductive organs, and gametes are formed due to this process. There are two types of meiosis. Meiosis-I, also termed reductional division, decreases the chromosome number to half (Lukhtanov et al. 2018). Meiosis-II is similar to mitotic division, a nuclear division process in which the parent cells split to yield two identical daughter cells in eukaryotic cells. The paper aims to shed light on the significance of meiosis, followed by the critical aspects of inheritance and inheritance patterns.

Gametes or sex cells are formed through meiosis, essential for sexual reproduction. The sporophytic information gets deactivated by meiosis, and genetic information for sex cell development gets activated by meiosis (Hisanaga et al. 2019). It preserves the number of chromosomes unchanged by halving it, and it is significant since the number of chromosomes doubles following fertilization. The process involves paternal and maternal chromosomes' independent assortment. As a result, the chromosomes and the traits they govern are reshuffled. Irregularities in meiosis cell division cause genetic mutation. Natural selection promotes beneficial mutations. A unique set of variations and traits are produced due to crossing over (Blount, Lenski and Losos 2018). Meiosis is believed to have four different biological functions. One is the widespread belief that sexual reproduction and recombination produce genetic variation upon which natural selection acts. Meiosis-induced recombination is crucial for repairing germline cells' genetic defects (Prieler et al. 2021). It is necessary for gamete reprogramming that gives rise to the fertilized egg. It contributes to maintaining the germ line's immortality through a rejuvenation process, including removing malfunctioning meiocytes or eliminating aberrant protein molecules and RNA. Chromosomes are the cells' mechanism of precisely assembling lengthy strands of DNA. Each parent contributes one set of chromosomes to non-sex cells. Sex cells with just one set of chromosomes are produced during meiosis (Wright and Diehl-Jones 2019). Human cells, for example, have 46 chromosomes, while eggs and sperms have 23 chromosomes each. A zygote is formed when each sex cell’s 23 chromosomes unite when an egg is fertilized by the sperm cell. The zygote contains 46 chromosomes, and it is a new cell. The first cell of any new individual is the zygote. One of the advantages of sexual reproduction is that it produces diversity within a population. Meiosis is responsible for the variation. Every sex cell produced from meiosis has a distinct combination of chromosomes. It signifies that no two egg or sperm cells are genetically similar. New traits' combinations are produced from every fertilization event. It explains why siblings have the same DNA as each other and their parents, but they are not identical.

Types of Meiosis

Numerous inheritance types like autosomal dominant, autosomal recessive, X-linked recessive, mitochondrial inheritance and X-linked dominant for single-gene diseases. In both complex multi-factorial diseases and single-gene diseases, the common phenomenon is genetic heterogeneity.

A genetic condition or trait can be passed down to the child from the parent through autosomal recessive inheritance. The term “autosomal” refers to a gene found on non-sex or one of the numbered chromosomes (Kirk and Tonkin 2021). When a child receives a single copy of each parent's altered or mutated gene, he or she has a genetic condition. Typically, neither of the parents of a kid with an autosomal recessive condition has the disease. Sickle cell anaemia is an illustration of an autosomal recessive condition. It means that in each cell, both gene copies are altered (Xu and Thein 2019). An individual with an autosomal recessive condition has a single copy of the defective gene in each parent, but they normally do not exhibit any symptoms.

Sickle cell anaemia (SCA) is a disorder in which faulty haemoglobin synthesis connects with other defective molecules of haemoglobin in the red blood cell (RBC), allowing the cell to distort abnormally. The cell's power to pass through narrow vascular channels is harmed, resulting in vascular bed obstruction and sludging, which leads to infarction and tissue ischemia. SCA impacts the structure of RBCs, which transports oxygen throughout the body (Chatterjee et al. 2018). RBCs are typically flexible and spherical, allowing them to pass through blood vessels easily. Some RBCs in SCA are shaped like crescent moons or sickles. The sickle cells become sticky and rigid, blocking or slowing blood flow. Sickle cell anemia is caused by a recessive allele, and sufferers are homozygous for the recessive allele. Due to RBC’s remarkable shortened life span, SCA patients or haemoglobin SS disease suffer from chronic complications. Glutamine is replaced by valine at haemoglobin’s beta chain sixth amino acid position, and as a result, haemoglobin S is formed (Harp et al. 2020). Individuals with haemoglobin S in a homozygous autosomal recessive manner (Hb SS) have sickle cell anaemia, while sickle trait is found in heterozygous individuals (Hb AS).

An autosomal dominant condition describes a condition resulting from a mutant gene or allele’s single copy, carried by one parent, that can impact both female and male offspring. An autosomal dominant condition can be caused by either parent’s single copy of the mutation (Wolf, Mitalipov and Mitalipov 2019). The phrase “dominant” suggests the fact that a disease-associated mutation’s single copy is sufficient to trigger the disease. On the contrary, a recessive disorder requires two copies of the mutation to develop the disease. An autosomal dominant’s condition’s classic example is Huntington's disease. It is a rare genetic disease in which the brain’s nerve cells progressively break down or deteriorate. Huntington’s disease impacts an individual’s functional abilities, frequently resulting in cognitive, movement, and psychiatric issues (Coppen and Roos 2017). Adult-onset, the most common type of Huntington’s disease, typically strikes individuals in their thirties or forties. Depression, irritability, poor coordination, involuntary movements, and difficulty making judgements or learning new information are some of the early indications of the disease. Chorea, an involuntary twitching or jerking condition, occurs in several individuals with Huntington’s disease (Coppen and Roos 2017). The movements grow more prominent as the disease advances. Individuals who are impacted experience difficulty speaking, walking, and swallowing. Changes in personality and degradation in reasoning and thinking abilities are the common symptoms of the condition. A juvenile type of Huntington’s disease that is less frequent occurs in adolescence or childhood (Quigley 2017). It includes issues with movement and emotional and mental changes. The juvenile form is characterized by clumsiness, slow mobility, stiffness, recurrent falls, drooling, and difficulty speaking.

Functions of Meiosis

Defects in the HTT gene are responsible for Huntington's disease. Huntington is a protein produced by the HTT gene that plays a critical role in brain nerve cells or neurons. The HTT mutation is caused by a DNA fragment known as a CAG trinucleotide repeat (Jimenez-Sanchez 2017). The segment comprises three DNA-building elements: guanine, adenine, and cytosine, which exist several times in a row. Within the gene, the CAG region is repeated roughly 10 to 35 times, while it is repeated 36 to over 120 times in people with Huntington's disease. A rise in the size of the CAG region is responsible for the formation of an unusually long Huntington protein variant (McColgan and Tabrizi 2018). The protein is then broken down into smaller, hazardous fragments that clump together and obstruct cell functioning. The malfunctioning and eventual death of the nerve cells in certain parts of the brain create the symptoms and signs of Huntington's disease.

 · A sex-linked condition- Haemophilia 

Sex-linked diseases are inherited through one of the Y or X chromosomes through families. The chromosomes X and Y are sex chromosomes. Dominant inheritance occurs when one parent's defective gene causes disease, whereas the other parent's gene is fine. The abnormal gene is the one that dominates. However, both matching genes are required to be abnormal for causing the disease in recessive inheritance. The disease is mild or does not arise if only one pair’s genes are abnormal. A carrier is someone who bears one defective gene but does not exhibit symptoms. Those with abnormal genes can pass them down to their offspring. "Sex-linked recessive" is the most popular term for X-linked recessive. Males are the most commonly impacted by X-linked recessive disorders (Houge, Black and Sergouniotis 2022). Males have only a single X chromosome. In males, the disease is produced by the X chromosomes’ single recessive gene, with the Y chromosome on the other half of the XY gene pair.

Nevertheless, the bulk of genes located on the X chromosome is absent from the Y chromosome. Therefore, it is incapable of protecting the male. A recessive gene on the X chromosome is responsible for haemophilia. Haemophilia is a bleeding disorder passed down the generations, where the blood cannot clot appropriately. It happens when there is no adequate clotting factor in the blood. A clotting factor is a blood protein that regulates bleeding. The most prevalent type, haemophilia A, also termed classical haemophilia, is characterized by reduced factor VIII levels (Aymonnier et al. 2021). Reduced levels of factor IX cause haemophilia B. In male individuals having one X chromosome, the gene’s single altered copy in each cell is adequate to trigger the disease. Females have two X chromosomes, and so for causing the disorder, a mutation must happen in the genes’ both copies. It is very unlikely that females would have haemophilia, as it is very unlikely that the gene will have two altered copies in females.

The sons cannot get X-linked traits from their fathers, which is a feature of X-linked inheritance. Females bearing a single copy of the gene are known as carriers. Internal bleeding is the most common type of bleeding. Reduced levels of clotting factors cause various bleeding episodes, most of which occur in the muscles or the joints. The bleeding episodes, commonly known as “bleeds”, can occur without any warning or due to injury or trauma (Puii, Maurya and Patil 2020). For helping with blood clots, specialized treatment is usually required, which is frequently injected or infused into a vein. Internal bleeding results in oedema and pain if not stopped promptly with treatment. Over time, bleeding into muscles and joints can result in permanent damage like chronic pain, arthritis, and joint damage that necessitates surgery.

Inheritance Patterns

 Essential aspects of inheritance determined by chromosomal genes

Thread-like structures called chromosomes are made up of protein and nucleic acids located within the living cells’ nucleus. They are primarily responsible for carrying genetic information in the form of genes. In the early 1900s, Sutton and Boveri proposed the chromosomal theory of inheritance. It is genetics’ fundamental theory (Portin and Wilkins 2017). According to the theory, genes found in the chromosomes are said to be the units of heredity. Long after Mendelian genetics, the chromosomal theory of inheritance was developed. Correns, De Vries and Tschermak discovered chromosomes present within the nucleus (Turnpenny, Ellard and Cleaver 2020). When the cells were divided, Boveri and Sutton observed chromosomes’ behaviour. They showed the chromosomes’ segregation during cell division’s Anaphase. The chromosomal theory of inheritance was established out of the notion of chromosomal segregation coupled with Mendelian principles. T.H. Morgan elaborated on the work by employing Drosophila melanogaster to demonstrate how sexual reproduction caused variations.

Conclusion 

Therefore, from the above discussion, it can be concluded that meiosis has great biological significance. There are numerous inheritance types like X-linked dominant, autosomal recessive, autosomal dominant and so on, and there are diseases associated with such conditions. The chromosomal theory of inheritance states that genes found in the chromosome are units of heredity. 

References

Aymonnier, K., Kawecki, C., Arocas, V., Boulaftali, Y. and Bouton, M.C., 2021. Serpins, new therapeutic targets for hemophilia. Thrombosis and Haemostasis, 121(03), pp.261-269.

Blount, Z.D., Lenski, R.E. and Losos, J.B., 2018. Contingency and determinism in evolution: Replaying life’s tape. Science, 362(6415), p.eaam5979.

Chatterjee, A., Agrawal, A., Adapa, D. and Sarangi, T.K., 2018. Sickle cell anaemia-a synopsis of the inherited ailment. Archives of medicine, 10(2), pp.0-0.

Coppen, E.M. and Roos, R.A., 2017. Current pharmacological approaches to reduce chorea in Huntington’s disease. Drugs, 77(1), pp.29-46.

Harp, K.O., Botchway, F., Dei-Adomakoh, Y., Wilson, M.D., Hood, J.L., Adjei, A.A., Stiles, J.K. and Driss, A., 2020. Hemoglobin Genotypes Modulate Inflammatory Response to Plasmodium Infection. Frontiers in Immunology, 11, p.3253.

Hisanaga, T., Yamaoka, S., Kawashima, T., Higo, A., Nakajima, K., Araki, T., Kohchi, T. and Berger, F., 2019. Building new insights in plant gametogenesis from an evolutionary perspective. Nature Plants, 5(7), pp.663-669.

Houge, S.D., Black, G.C. and Sergouniotis, P.I., 2022. Genetic disorders and genetic variants. In Clinical Ophthalmic Genetics and Genomics (pp. 1-5). Academic Press.

Jimenez-Sanchez, M., Licitra, F., Underwood, B.R. and Rubinsztein, D.C., 2017. Huntington’s disease: mechanisms of pathogenesis and therapeutic strategies. Cold Spring Harbor perspectives in medicine, 7(7), p.a024240.

Kallen, A.N., 2020. Basic genetics: mitosis, meiosis, chromosomes, DNA, RNA, and beyond. In Human Reproductive Genetics (pp. 3-16). Academic Press.

Kirk, M. and Tonkin, E., 2021. Inherited conditions and the family. A Textbook of Children's and Young People's Nursing-E-Book, p.124.

Legato, M.J., 2020. What determines biological sex?. In The Plasticity of Sex (pp. 1-23). Academic Press.

Lukhtanov, V.A., Dinc?, V., Friberg, M., Šíchová, J., Olofsson, M., Vila, R., Marec, F. and Wiklund, C., 2018. Versatility of multivalent orientation, inverted meiosis, and rescued fitness in holocentric chromosomal hybrids. Proceedings of the National Academy of Sciences, 115(41), pp.E9610-E9619.

McColgan, P. and Tabrizi, S.J., 2018. Huntington's disease: a clinical review. European journal of neurology, 25(1), pp.24-34.

Portin, P. and Wilkins, A., 2017. The evolving definition of the term “gene”. Genetics, 205(4), pp.1353-1364.

Prieler, S., Chen, D., Huang, L., Mayrhofer, E., Zsótér, S., Vesely, M., Mbogning, J. and Klein, F., 2021. Spo11 generates gaps through concerted cuts at sites of topological stress. Nature, 594(7864), pp.577-582.

Puii, L., Maurya, A. and Patil, M., 2020. TO ASSESS THE EFFECTIVENESS OF SELF INSTRUCTIONAL MODULE (SIM) ON KNOWLEDGE REGARDING HAEMOPHILIA IN CHILDREN AMONG SCHOOL TEACHERS. International Journal of Modern Agriculture, 9(3), pp.6-10.

Quigley, J., 2017. Juvenile Huntington’s disease: diagnostic and treatment considerations for the psychiatrist. Current psychiatry reports, 19(2), pp.1-4.

Turnpenny, P.D., Ellard, S. and Cleaver, R., 2020. Emery's Elements of Medical Genetics E-Book. Elsevier Health Sciences.

Wolf, D.P., Mitalipov, P.A. and Mitalipov, S.M., 2019. Principles of and strategies for germline gene therapy. Nature medicine, 25(6), pp.890-897.

Wright, K. and Diehl-Jones, W., 2019. An Introduction to Clinical Genetics. Neonatal Network, 38(5), pp.266-273.

Xu, J.Z. and Thein, S.L., 2019. The carrier state for sickle cell disease is not completely harmless. Haematologica, 104(6), p.1106.

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