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Chromosome Pairing and Fertility in Mice
Published in Christopher B. Gillies, Fertility and Chromosome Pairing: Recent Studies in Plants and Animals, 2020
Sex chromosome pairing as a means of estimating the substages of pachytene has been treated in Section III. For a complete account in mammals (and birds), the reader is referred to chapter 3 in this volume. The concern here is that the sex chromosomes are the only ones for which the effects of an absence of meiotic pairing can be studied for their own value. In autosomal situations, as we have seen extensively in the sections dealing with the various chromosome mutations, unpaired chromosomes or segments almost always aggregate with the sex chromosome axial elements. Sex chromosome univalence at pachytene is generally taken to be cell lethal at the first meiotic division and cells seem to succumb at metaphase I (see Reference 10 for additional citations). In a situation where the extent of synapsis between the sex chromosomes was decreased (a finding which accompanies sex chromosome univalence of part of the primary spermatocytes), increased frequencies of severely malformed spermatozoa were found.88 Moreover, when pairing is more severely affected, as in XOSxr mice that carry the male-determining sequences of a Y chromosomal fragment in the distal telomeric region of the X chromosome, increased frequencies of abnormal spermatozoa (besides a majority of diploid spermatozoa) are observed.95 Abnormal pairing is achieved here by nonhomologous meiotic pairing between the proximal and distal segments of the XSxr chromosome: ring formation.
Preimplantation Genetic Testing for Structural Rearrangements
Published in Darren K. Griffin, Gary L. Harton, Preimplantation Genetic Testing, 2020
Homologous pairing and recombination play a critical role in meiosis. In a normal individual, during the pachytene stage of meiosis I, each chromosome pairs with its homolog and they are held together until they are segregated properly to the poles at the end of anaphase. However, in RecT carriers, in order to allow homologous synapsis to occur, the four chromosomes (two derivatives and two normal homologs) form a “quadrivalent” (Figure 4.3). During anaphase I, there are five major possibilities for segregation of those chromosomes: alternate, adjacent-1, adjacent-2, 3:1, and 4:0 (Figure 4.4). With the addition of the recombination events within the segments resulting in asymmetric segregation in meiosis II and meiotic non-disjunctions in anaphase II, up to 32 different gametes could be produced, of which only 2 arising from alternate segregation could give rise to normal/balanced embryos (Table 4.1) (reviewed in [20]).
Genetics of mammalian meiosis
Published in C. Yan Cheng, Spermatogenesis, 2018
The prophase I is further divided into substages largely based on the morphology of the synaptonemal complex: leptotene, zygotene, pachytene, and diplotene. At the leptotene stage, synaptonemal complex proteins form axial elements (AEs) along chromosomal axes but synapsis is not yet formed. At the zygotene stage, chromosomal synapsis is initiated but incomplete. At this stage, CE and TF components connect the two AEs and thus only localize to the synapsed regions. AEs are called LEs in synapsis. The subsequent pachytene stage is characterized by full synapsis along the entire length of all pairs of homologous chromosomes except for the X-Y chromosomes in male germ cells. At the diplotene stage, CE and TF components begin to disassemble from SCs to cause desynapsis of homologous chromosomes.
Sperm quality and testicular histopathology of Wistar albino male rats treated with hydroethanolic extract of Cordia dichotoma fruits
Published in Pharmaceutical Biology, 2022
Samah A. El-Newary, Mohamed S. Aly, Amal R. Abd El Hameed, Mohamed S. Kotp, Abdelghany A. Youssef, Naglaa A. Ali
Indeed, sperm production is strongly associated with TC on the excellent mass production of germ cells during spermatogenesis. Therefore, TC de novo synthesis was elevated during the development of pachytene, leptotene, and zygotene stages to increase germ cells' diameter and surface area (Sèdes et al. 2018). Then TC synthesis decreased, and TC hydrolysed to cholesterol ester by the hormone-sensitive lipase (HSL), which involves in spermatids and spermatozoa elongation. Therefore, any disruption in lipid metabolism during sperm production can lead to arrest cell differentiation. Spermatozoa, like any animal cell, have a lipid bilayer plasma membrane. Polyunsaturated fatty acids (PUFAs) make spermatozoon more viable and dynamic (Sèdes et al. 2018). Germ cells produce TC by de novo and supply with TC in the seminiferous tubules to increase their membrane surface (Akpovi et al. 2006).
Genetic variations as molecular diagnostic factors for idiopathic male infertility: current knowledge and future perspectives
Published in Expert Review of Molecular Diagnostics, 2021
Mohammad Karimian, Leila Parvaresh, Mohaddeseh Behjati
The synaptonemal complex is an important component for chromosome pairing, segregation, and recombination. Hormad1 is essential for mammalian gametogenesis because male knockout mice are infertile. Hormad1-deficient testes in the early stages of pachytene show meiosis arrest without demonstration of synaptonemal complexes [152]. To analyze the hypothesis that human HORMAD1 gene defect is associated with human azoospermia induced by meiosis arrest, mutation analysis in all coding regions was performed by Miyamoto et al. By sequence analysis, SNP1 (163A> G), SNP2 (501T>G) and SNP3 (918C>T) were found in exons 3, 8, and 10. Both SNP1 and SNP2 were associated with human azoospermia resulting from the complete arrest of primary meiosis. They suggested that HORMAD1 has an essential mitotic function in human spermatogenesis [153].
Interaction of the mTERT telomerase catalytic subunit with the c-Abl tyrosine kinase in mouse granulosa cells
Published in Journal of Receptors and Signal Transduction, 2020
Aylin Yaba, Sami Agus, Ecem Yıldırım, Cihan Süleyman Erdogan, Bayram Yılmaz
Thus far, only a few studies have investigated the regulation of mTERT in granulosa cells; additionally, the underlying molecular mechanisms of this regulation are poorly understood for c-Abl. Studies with c-Abl homozygous knockout cells shown that c-Abl regulates telomere length and c-Abl deficient cells have a critical role in the negative regulation of human TERT [37]. Some defects at the pachytene stage during spermatogenesis were observed in a study with c-Abl knockout mice [38]. c-Abl protein is located at the ends of pachytene chromosomes in early meiosis metaphase I spermatocytes [39]. Therefore, this is probably why c-Abl protein can contact with telomerase in mitotic cells [38]. Extension of telomere in c-Abl homozygous knockout cells shows that c-Abl has a very important role in the regulation of telomerase function in the relation between c-Abl and human TERT [27].