Ben May Department for Cancer Research, University of Chicago, Chicago, IL 60637, USA.
Genetics. 2013 Feb;193(2):633-49. doi: 10.1534/genetics.112.146647. Epub 2012 Nov 19.
ETS family transcription factors are evolutionarily conserved downstream effectors of Ras/MAPK signaling with critical roles in development and cancer. In Drosophila, the ETS repressor Yan regulates cell proliferation and differentiation in a variety of tissues; however, the mechanisms of Yan-mediated repression are not well understood and only a few direct target genes have been identified. Yan, like its human ortholog TEL1, self-associates through an N-terminal sterile α-motif (SAM), leading to speculation that Yan/TEL1 polymers may spread along chromatin to form large repressive domains. To test this hypothesis, we created a monomeric form of Yan by recombineering a point mutation that blocks SAM-mediated self-association into the yan genomic locus and compared its genome-wide chromatin occupancy profile to that of endogenous wild-type Yan. Consistent with the spreading model predictions, wild-type Yan-bound regions span multiple kilobases. Extended occupancy patterns appear most prominent at genes encoding crucial developmental regulators and signaling molecules and are highly conserved between Drosophila melanogaster and D. virilis, suggesting functional relevance. Surprisingly, although occupancy is reduced, the Yan monomer still makes extensive multikilobase contacts with chromatin, with an overall pattern similar to that of wild-type Yan. Despite its near-normal chromatin recruitment, the repressive function of the Yan monomer is significantly impaired, as evidenced by elevated target gene expression and failure to rescue a yan null mutation. Together our data argue that SAM-mediated polymerization contributes to the functional output of the active Yan repressive complexes that assemble across extended stretches of chromatin, but does not directly mediate recruitment to DNA or chromatin spreading.
ETS 家族转录因子是 Ras/MAPK 信号下游的进化保守效应因子,在发育和癌症中发挥着关键作用。在果蝇中,ETS 抑制因子 Yan 在各种组织中调节细胞增殖和分化;然而,Yan 介导的抑制机制尚不清楚,并且只鉴定了少数直接靶基因。Yan 与其人类同源物 TEL1 一样,通过 N 端无菌 α 基序(SAM)自我缔合,这导致人们推测 Yan/TEL1 聚合物可能沿着染色质扩散形成大的抑制域。为了验证这一假说,我们通过重组一个点突变来创建 Yan 的单体形式,该突变阻止了 SAM 介导的自缔合,并将其插入 yan 基因组座,然后将其全基因组染色质占有率与内源性野生型 Yan 的占有率进行比较。与扩散模型的预测一致,野生型 Yan 结合的区域跨越多个千碱基。扩展的占有模式在编码关键发育调节剂和信号分子的基因中最为明显,并且在果蝇和 D. virilis 之间高度保守,这表明它们具有功能相关性。令人惊讶的是,尽管 Yan 单体的占有率降低,但它仍然与染色质进行广泛的多千碱基接触,整体模式与野生型 Yan 相似。尽管 Yan 单体的染色质募集接近正常,但它的抑制功能明显受损,这表现为靶基因表达升高,并且无法挽救 yan 缺失突变。总的来说,我们的数据表明,SAM 介导的聚合作用有助于 Yan 抑制复合物的功能性输出,这些复合物在扩展的染色质上组装,但不会直接介导对 DNA 的招募或染色质的扩散。