Temasek Life Sciences Laboratory, Singapore.
EMBO J. 2011 Feb 16;30(4):744-55. doi: 10.1038/emboj.2010.344. Epub 2011 Jan 7.
We have analysed the role of RBR (retinoblastoma related), the Arabidopsis homologue of the tumour suppressor Retinoblastoma protein (pRb), during meiosis. We characterise the rbr-2 mutation, which causes a loss of RBR in male meiocytes. The rbr-2 plants exhibit strongly reduced fertility, while vegetative growth is generally unaffected. The reduced fertility is due to a meiotic defect that results in reduced chiasma formation and subsequent errors in chromosome disjunction. Immunolocalisation studies in wild-type meiocytes reveal that RBR is recruited as foci to the chromosomes during early prophase I in a DNA double-strand-break-dependent manner. In the absence of RBR, expression of several meiotic genes is reduced. The localisation of the recombinases AtRAD51 and AtDMC1 is normal. However, localisation of the MutS homologue AtMSH4 is compromised. Additionally, polymerisation of the synaptonemal complex protein AtZYP1 is abnormal. Together, these data indicate that loss of RBR during meiosis results in a reduction of crossover formation and an associated failure in chromosome synapsis. Our results indicate that RBR has an important role in meiosis affecting different aspects of this complex process.
我们分析了 RBR(视网膜母细胞瘤相关)在减数分裂过程中的作用,RBR 是拟南芥同源物肿瘤抑制蛋白 Retinoblastoma(pRb)。我们描述了 rbr-2 突变,该突变导致雄性减数分裂细胞中 RBR 的丢失。rbr-2 植株表现出严重的不育性,而营养生长通常不受影响。这种不育性是由于减数分裂缺陷导致的,该缺陷导致交叉形成减少,随后染色体分离错误。在野生型减数分裂细胞中的免疫定位研究表明,RBR 作为焦点在早期粗线期以依赖于 DNA 双链断裂的方式被募集到染色体上。在没有 RBR 的情况下,几个减数分裂基因的表达减少。重组酶 AtRAD51 和 AtDMC1 的定位正常。然而,MutS 同源物 AtMSH4 的定位受损。此外,联会复合体蛋白 AtZYP1 的聚合也异常。这些数据表明,减数分裂过程中 RBR 的丢失导致交叉形成减少,并与染色体联会失败相关。我们的结果表明,RBR 在减数分裂中具有重要作用,影响这个复杂过程的不同方面。