The association of ATR protein with mouse meiotic chromosome cores

被引:0
|
作者
Peter B. Moens
Madalena Tarsounas
Takashi Morita
Toshiyuki Habu
Scott T. Rottinghaus
Raimundo Freire
Stephen P. Jackson
Carrolee Barlow
Anthony Wynshaw-Boris
机构
[1] Department of Biology,
[2] York University,undefined
[3] Toronto,undefined
[4] Ontario,undefined
[5] M3J 1P3,undefined
[6] Canada,undefined
[7] Department of Molecular Embryology,undefined
[8] Osaka University,undefined
[9] Osaka 565,undefined
[10] Japan,undefined
[11] Wellcome/CRC Institute,undefined
[12] Cambridge CB2 1QR,undefined
[13] UK,undefined
[14] Genetic Disease Research Branch,undefined
[15] NHGRI,undefined
[16] NIH,undefined
[17] Bethesda,undefined
[18] MD 20892-4470,undefined
[19] USA,undefined
来源
Chromosoma | 1999年 / 108卷
关键词
Chromosome Pairing; Electron Microscope Observation; Synaptonemal Complex; Meiotic Prophase; Meiotic Chromosome;
D O I
暂无
中图分类号
学科分类号
摘要
The ATR (ataxia telangiectasia- and RAD3-related) protein is present on meiotic prophase chromosome cores and paired cores (synaptonemal complexes, SCs). Its striking characteristic is that the protein forms dense aggregates on the cores and SCs of the last chromosomes to pair at the zygotene-pachytene transition. It would appear that the ATR protein either signals delays in pairing or it is directly involved in the completion of the pairing phase. Atm-deficient spermatocytes, which are defective in the chromosome pairing phase, accumulate large amounts of ATR. The behaviour of ATR at meiotic prophase sets it apart from the distribution of the RAD51/DMC1 recombinase complex and our electron microscope observations confirm that they do not co-localize. We failed to detect ATM in association with cores/SCs and we have reported elsewhere that RAD1 protein does not co-localize with DMC1 foci. The expectation that putative DNA-damage checkpoint proteins, ATR, ATM and RAD1, are associated with RAD51/DMC1 recombination sites where DNA breaks are expected to be present, is therefore not supported by our observations.
引用
收藏
页码:95 / 102
页数:7
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