Smirnova Natalya A, Romanienko Peter J, Khil Pavel P, Camerini-Otero R Daniel
Genetics and Biochemistry Branch, NIDDK, National Institutes of Health, 5 Memorial Drive, Bethesda, Maryland 20892, USA.
Reproduction. 2006 Jul;132(1):67-77. doi: 10.1530/rep.1.00997.
Spo11, a meiosis-specific protein, introduces double-strand breaks on chromosomal DNA and initiates meiotic recombination in a wide variety of organisms. Mouse null Spo11 spermatocytes fail to synapse chromosomes and progress beyond the zygotene stage of meiosis. We analyzed gene expression profiles in Spo11(-/ -)adult and juvenile wild-type testis to describe genes expressed before and after the meiotic arrest resulting from the knocking out of Spo11. These genes were characterized using the Gene Ontology data base. To focus on genes involved in meiosis, we performed comparative gene expression analysis of Spo11(-/ -)and wild-type testes from 15-day mice, when spermatocytes have just entered pachytene. We found that the knockout of Spo11 causes dramatic changes in the level of expression of genes that participate in meiotic recombination (Hop2, Brca2, Mnd1, FancG) and in the meiotic checkpoint (cyclin B2, Cks2), but does not affect genes encoding protein components of the synaptonemal complex. Finally, we discovered unknown genes that are affected by the disruption of the Spo11 gene and therefore may be specifically involved in meiosis and spermatogenesis.
Spo11是一种减数分裂特异性蛋白,可在染色体DNA上引入双链断裂,并在多种生物体中启动减数分裂重组。小鼠缺失Spo11的精母细胞无法使染色体联会,减数分裂无法超越偶线期。我们分析了Spo11基因敲除的成年和幼年野生型小鼠睾丸中的基因表达谱,以描述在Spo11敲除导致的减数分裂停滞前后表达的基因。这些基因使用基因本体数据库进行了表征。为了聚焦于参与减数分裂的基因,我们对15日龄小鼠(此时精母细胞刚进入粗线期)的Spo11基因敲除小鼠和野生型小鼠睾丸进行了比较基因表达分析。我们发现,Spo11基因敲除会导致参与减数分裂重组的基因(Hop2、Brca2、Mnd1、FancG)以及减数分裂检查点基因(细胞周期蛋白B2、Cks2)的表达水平发生显著变化,但不影响编码联会复合体蛋白成分的基因。最后,我们发现了一些受Spo11基因破坏影响的未知基因,因此这些基因可能特别参与减数分裂和精子发生。