Parvanov Emil, Kohli Juerg, Ludin Katja
Institute of Cell Biology, University of Bern, CH-3012 Bern, Switzerland.
Genetics. 2008 Dec;180(4):1859-68. doi: 10.1534/genetics.108.093005. Epub 2008 Oct 9.
The mating-type bias (mat-bias) of gene conversion was previously described as a phenomenon in which the number of prototrophic recombinants in an ura4A heteroallelic two-factor cross relates to the mating types of the parents. We show now that the mat-bias is restricted neither to ura4A nor to recombination hotspots, but occurs at other genomic loci, too. It is specific for gene conversion and absent in azygotic meiosis. Thus, the mat-bias must originate from mating-type-specific "imprinting" events before karyogamy takes place. Structural variations of the mating-type locus, such as h(+N), h(+S), h(-S), h(+smtDelta), or h(-smtDelta), showed mat-bias manifestation. Mutations in genes coding for histone acetylase (gcn5, ada2) and histone deacetylase (hos2, clr6) activities smooth or abolish the mat-bias. In addition, the mat-bias depends on the presence of Swi5. We propose a new role for Swi5 and the histone acetylation status in mat-bias establishment through directionality of repair from the intact chromatid to the broken chromatid.
基因转换的交配型偏向(mat-bias)先前被描述为一种现象,即在ura4A异等位双因子杂交中,原养型重组体的数量与亲本的交配型相关。我们现在表明,mat-bias既不限于ura4A,也不限于重组热点,在其他基因组位点也会发生。它是基因转换所特有的,在非合子减数分裂中不存在。因此,mat-bias必定源自核配发生之前交配型特异性的“印记”事件。交配型位点的结构变异,如h(+N)、h(+S)、h(-S)、h(+smtDelta)或h(-smtDelta),表现出mat-bias。编码组蛋白乙酰化酶(gcn5、ada2)和组蛋白去乙酰化酶(hos2、clr6)活性的基因突变会使mat-bias变平缓或消除。此外,mat-bias依赖于Swi5的存在。我们提出Swi5和组蛋白乙酰化状态在通过从完整染色单体到断裂染色单体的修复方向性建立mat-bias中具有新作用。