what will you call the x and y chromosome homologous or non homologous
Answers
Homologous chromosomes are the same length and have specific nucleotide segmentscalled genes in exactly the same location, or locus.
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The XX/XY sex chromosomal system of mammals, including human, challenges the chromosome pairing mechanism during male meiosis. Pairing and subsequent separation of homologous chromosomes generates haploid cells from diploid cells during the meiotic divisions. One of the basic requirements for recognition between homologous chromosomes is DNA sequence identity. Since the X and Y chromosome share little homology, their quest for each other is difficult, and has special characteristics. During the lengthy meiotic prophase, all autosomal chromosomes synapse, by forming a special protein structure called the synaptonemal complex, which connects the chromosomal axes. In contrast, the X and Y chromosome synapse only in the short homologous pseudoautosomal regions, and form the so-called XY body.1 In this specialized chromatin area, transcription is shut down by a mechanism named meiotic sex chromosome inactivation (MSCI) (reviewed by Refs. 2 and 3). The sex chromosomes remain silent throughout the rest of meiotic prophase, and only few sex-linked genes are (re)activated in postmeiotic spermatids.2 Since long, scientists have wondered how MSCI is achieved, and what its biological significance is.
Recently, two papers4, 5 significantly increased our understanding of how and why MSCI works.
So far, the only molecule that was known to be absolutely essential for initiation of MSCI was γH2AX.6 This phosphorylated form of histone H2AX marks the XY body from its formation until diplotene in mouse.7 In mice lacking H2AX, no XY body is formed, the sex chromosomes are not silenced and meiosis arrests at pachytene.6 The phosphorylation of H2AX at the XY body is mediated by the checkpoint kinase ATR that can be visualized along the unsynapsed axes of X and Y from late zygotene onwards.8 In their recent paper, Ichijima et al.4 reveal that the phosphorylation of H2AX occurs in two phases; first, it is restricted to the chromosomal axes, then the area extends, and H2AX also becomes phosphorylated in the surrounding chromatin loops. This second phase, when γH2AX spreads, depends on a protein named mediator of DNA damage checkpoint 1 (MDC1), and this function is required for transcriptional silencing of the sex . MDC1 is a known binding partner of γH2AX,9, 10 and both proteins, as well as ATR, are well known for their role in the DNA damage response pathway in somatic cells. This pathway plays a pivotal role in sensing the presence of single-stranded DNA at stalled replication fork to allow repair as well as activation of cell cycle checkpoints. Interestingly, the authors also analyzed the role of MDC1 in somatic cells. In analogy to their observations in meiotic cells, they observed reduced amplification of ATR-dependent γH2AX signals after replicative stress in the absence of MDC1, compared to control cells. They also showed that RNA polymerase II is excluded from chromatin at replication-stalled sites that are marked by ATR- and MDC1-dependent γH2AX accumulation, thereby confirming and extending the observations described by Shanbag et al.,11 who discovered that DNA double-strand breaks (DSBs) elicit transcriptional silencing in cis. These data reveal an analogy between somatic and meiotic cells, with respect to the link between DNA repair and DNA damage response protein accumulation (at respectively DNA damage sites and unsynapsed axes), and transcriptional silencing. It should be noted that 200–400 enzymatically generated DSBs are induced at the onset of meiotic prophase, to mediate homology recognition and meiotic recombination. Meiotic DSBs are also induced in the non-homologous regions of X and Y, and DSB repair molecules are present on the unsynapsed X chromosomal axis.12 Together with the observation that meiotic silencing is impaired when repair of meiotic DSBs is hampered,13 this indicates that MSCI is also mechanistically related to DSB repair and the DNA damage response pathway in somatic cells