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10.1101/sqb.2017.82.034298 http://scihub22266oqcxt.onion/10.1101/sqb.2017.82.034298 C6041145!6041145 !29440567     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29440567 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cold+Spring+Harb+Symp+Quant+Biol 2017 ; 82 (ä): 249-257 Nephropedia Template TP {{tp|p=29440567 |t=2017. Cellular and Molecular Mechanisms of Centromere Drive |pdf=|usr=}}{{29440567 }} gab.com Text Cellular and Molecular Mechanisms of Centromere Drive JO: Cold Spring Harb Symp Quant Biol http://www.kidney.de/pget.php?&tw=1&pmid=29440567 #FOAvip The asymmetric outcome of female meiosis I, whereby an entire set of chromosomes are discarded into a polar body, presents an opportunity for selfish genetic elements to cheat the process and disproportionately segregate to the egg. Centromeres, the chromosomal loci that connect to spindle microtubules, could potentially act as selfish elements and "drive" in meiosis. We review the current understanding of the genetic and epigenetic contributions to centromere identity and describe recent progress in a powerful model system to study centromere drive in mice. The progress includes mechanistic findings regarding two main requirements for a centromere to exploit the asymmetric outcome of female meiosis. The first is an asymmetry between centromeres of homologous chromosomes, and we found this is accomplished through massive changes in the abundance of the repetitive DNA underlying centromeric chromatin. The second requirement is an asymmetry in the meiotic spindle, which is achieved through signaling from the oocyte cortex that leads to asymmetry in a posttranslational modification of tubulin, tyrosination. Together, these two asymmetries culminate in the biased segregation of expanded centromeres to the egg, and we describe a mechanistic framework to understand this process. Twit Text FOAVip Cellular and Molecular Mechanisms of Centromere Drive ????Cold Spring Harb Symp Quant Biol http://www.kidney.de/pget.php?&tw=1&pmid=29440567 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29440567 #FOAvip English Wikipedia <ref>{{Cite pmid|29440567 }}</ref> Cellular and Molecular Mechanisms of Centromere Drive #MMPMID29440567 Lampson MA ; Black BE Cold Spring Harb Symp Quant Biol 2017[]; 82 (ä): 249-257 PMID29440567 show ga The asymmetric outcome of female meiosis I, whereby an entire set of chromosomes are discarded into a polar body, presents an opportunity for selfish genetic elements to cheat the process and disproportionately segregate to the egg. Centromeres, the chromosomal loci that connect to spindle microtubules, could potentially act as selfish elements and "drive" in meiosis. We review the current understanding of the genetic and epigenetic contributions to centromere identity and describe recent progress in a powerful model system to study centromere drive in mice. The progress includes mechanistic findings regarding two main requirements for a centromere to exploit the asymmetric outcome of female meiosis. The first is an asymmetry between centromeres of homologous chromosomes, and we found this is accomplished through massive changes in the abundance of the repetitive DNA underlying centromeric chromatin. The second requirement is an asymmetry in the meiotic spindle, which is achieved through signaling from the oocyte cortex that leads to asymmetry in a posttranslational modification of tubulin, tyrosination. Together, these two asymmetries culminate in the biased segregation of expanded centromeres to the egg, and we describe a mechanistic framework to understand this process. äCellular and Molecular Mechanisms of Centromere Drive (epmc).pdf DeepDyve Pubget Overpricing