Burgess S M, Kleckner N, Weiner B M
Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA.
Genes Dev. 1999 Jun 15;13(12):1627-41. doi: 10.1101/gad.13.12.1627.
FISH analysis of well-spread chromosomes reveals that homologs are paired in vegetatively growing budding yeast diploid cells, via multiple interstitial interactions, and independent of recA homologs and mating type heterozygosity. Pairing is present during G1 and G2, and in cells arrested at G1 by mating pheromone, but is disrupted during S phase. Thus, somatic pairing is qualitatively analogous to premeiotic and early meiotic pairing. S-phase pairing disruption occurs by a complex intranuclear program involving regional, nucleus-wide, and temporal determinants. Pairing is also disrupted in two G2-arrest conditions (cdc13ts and nocodazole). Together these findings suggest that cell cycle signals may provoke pairing disruption by modulating underlying chromosome and/or chromatin structure. Whether the cell chooses to disrupt pairing contacts or not (e.g., S phase and G2 arrest, but not G1 arrest or normal G1 or G2), could be dictated by functional considerations involving homolog/sister discrimination.
对伸展良好的染色体进行荧光原位杂交(FISH)分析表明,在营养生长的出芽酵母二倍体细胞中,同源染色体通过多种居间相互作用配对,且与RecA同源物和交配型杂合性无关。配对在G1期和G2期存在,在被交配信息素阻滞在G1期的细胞中也存在,但在S期被破坏。因此,体细胞配对在性质上类似于减数分裂前和减数分裂早期的配对。S期配对的破坏是由一个复杂的核内程序引起的,该程序涉及区域、全核和时间决定因素。在两种G2期阻滞条件下(cdc13ts和诺考达唑)配对也被破坏。这些发现共同表明,细胞周期信号可能通过调节潜在的染色体和/或染色质结构来引发配对的破坏。细胞是否选择破坏配对接触(例如,S期和G2期阻滞,但不是G1期阻滞或正常的G1期或G2期),可能由涉及同源物/姐妹鉴别功能的因素决定。