Institute of Innovative Research, Tokyo Institute of Technology, Tokyo, Japan.
School of Life Science and Technology, Department of Life Science and Technology, Tokyo Institute of Technology, Tokyo, Japan.
PLoS Genet. 2018 May 31;14(5):e1007424. doi: 10.1371/journal.pgen.1007424. eCollection 2018 May.
Mating-type switching in Schizosaccharomyces pombe entails programmed gene conversion events regulated by DNA replication, heterochromatin, and the HP1-like chromodomain protein Swi6. The whole mechanism remains to be fully understood. Using a gene deletion library, we screened ~ 3400 mutants for defects in the donor selection step where a heterochromatic locus, mat2-P or mat3-M, is chosen to convert the expressed mat1 locus. By measuring the biases in mat1 content that result from faulty directionality, we identified in total 20 factors required for donor selection. Unexpectedly, these included the histone H3 lysine 4 (H3K4) methyltransferase complex subunits Set1, Swd1, Swd2, Swd3, Spf1 and Ash2, the BRE1-like ubiquitin ligase Brl2 and the Elongator complex subunit Elp6. The mutant defects were investigated in strains with reversed donor loci (mat2-M mat3-P) or when the SRE2 and SRE3 recombination enhancers, adjacent to the donors, were deleted or transposed. Mutants in Set1C, Brl2 or Elp6 altered balanced donor usage away from mat2 and the SRE2 enhancer, towards mat3 and the SRE3 enhancer. The defects in these mutants were qualitatively similar to heterochromatin mutants lacking Swi6, the NAD+-dependent histone deacetylase Sir2, or the Clr4, Raf1 or Rik1 subunits of the histone H3 lysine 9 (H3K9) methyltransferase complex, albeit not as extreme. Other mutants showed clonal biases in switching. This was the case for mutants in the NAD+-independent deacetylase complex subunits Clr1, Clr2 and Clr3, the casein kinase CK2 subunit Ckb1, the ubiquitin ligase component Pof3, and the CENP-B homologue Cbp1, as well as for double mutants lacking Swi6 and Brl2, Pof3, or Cbp1. Thus, we propose that Set1C cooperates with Swi6 and heterochromatin to direct donor choice to mat2-P in M cells, perhaps by inhibiting the SRE3 recombination enhancer, and that in the absence of Swi6 other factors are still capable of imposing biases to donor choice.
在裂殖酵母中,交配型转换需要经过编程的基因转换事件,这些事件受 DNA 复制、异染色质和 HP1 样染色质域蛋白 Swi6 调控。然而,整个机制仍有待充分理解。我们使用基因缺失文库筛选了大约 3400 个突变体,以寻找在供体选择步骤中出现缺陷的突变体,在这个步骤中,一个异染色质位点 mat2-P 或 mat3-M 被选择来转换表达的 mat1 基因座。通过测量由于方向性错误导致的 mat1 含量的偏差,我们总共鉴定了 20 个参与供体选择的因子。出乎意料的是,这些因子包括组蛋白 H3 赖氨酸 4(H3K4)甲基转移酶复合物亚基 Set1、Swd1、Swd2、Swd3、Spf1 和 Ash2、BRE1 样泛素连接酶 Brl2 和 Elongator 复合物亚基 Elp6。我们在反转供体基因座(mat2-M mat3-P)的菌株中或当相邻供体的 SRE2 和 SRE3 重组增强子缺失或易位时,对这些突变体的缺陷进行了研究。Set1C、Brl2 或 Elp6 的突变体改变了平衡的供体使用,偏离了 mat2 和 SRE2 增强子,偏向了 mat3 和 SRE3 增强子。这些突变体的缺陷与缺乏 Swi6、依赖 NAD+的组蛋白去乙酰化酶 Sir2 或组蛋白 H3 赖氨酸 9(H3K9)甲基转移酶复合物的 Clr4、Raf1 或 Rik1 亚基的异染色质突变体相似,但没有那么极端。其他突变体表现出克隆转换偏倚。这种情况发生在 NAD+-非依赖性去乙酰化酶复合物亚基 Clr1、Clr2 和 Clr3、酪蛋白激酶 CK2 亚基 Ckb1、泛素连接酶成分 Pof3 和着丝粒 B 同源物 Cbp1 的突变体中,以及缺乏 Swi6 和 Brl2、Pof3 或 Cbp1 的双突变体中。因此,我们提出 Set1C 与 Swi6 和异染色质合作,指导 M 细胞中 mat2-P 的供体选择,可能是通过抑制 SRE3 重组增强子,并且在缺乏 Swi6 的情况下,其他因子仍然能够对供体选择施加偏倚。