The proline-rich domain of MML-1 is biologically important but not required for localization to target promoters.
The proline-rich domain of MML-1 is biologically important but not required for localization to target promoters.
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DOI：
10.17912/micropub.biology.000498
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发表时间：
2021
影响因子：
--
通讯作者：
Grishok A
中科院分区：
文献类型：
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作者：
Ceballos A;Esse R;Grishok A
MYC超家族转录因子在C. MML-1（Myc和Mondo-like 1）在多种模型中显示出促进寿命延长，并调节C. elegans发育这项先前的研究没有涉及MML-1的分子表征。在这里，我们使用可用的mml-1突变等位基因和其他试剂来证明，MML-1被O-GlcNAc修饰，与DOT-1.1组蛋白甲基转移酶复合物直接调控的一些基因的启动子结合，并在促进神经元迁移中发挥作用。令人惊讶的是，我们发现，缺失等位基因mml-1（ok 849），这被认为是一个空的，产生一个内部截短的蛋白质产生的框内缺失。该截短产物定位于MML-1靶启动子未受损。MML-1的缺失区域富含脯氨酸，并且其在MML-1的哺乳动物同源物中的功能知之甚少。基于我们的工作和以前发表的数据，我们得出结论，MML-1的内部富含脯氨酸的区域是DNA结合的障碍，但具有生物学重要性。
The only representative of the MYC superfamily transcription factors in C. elegans, MML-1 (Myc and Mondo-like 1), was shown to promote extended lifespan in a variety of models and to regulate some aspects of C. elegans development. This previous research did not involve molecular characterization of MML-1. Here we use available mml-1 mutant alleles and other reagents to demonstrate that MML-1 is modified by O-GlcNAc, binds to promoters of some genes directly regulated by the DOT-1.1 histone methyltransferase complex, and has a role in promoting neuronal migration. Surprisingly, we found that the deletion allele mml-1(ok849), which was considered a null, produces an internally truncated protein resulting from an in-frame deletion. Localization of this truncated product to MML-1 target promoters was not impaired. The deleted region of MML-1 is proline-rich, and its function is poorly understood in mammalian homologs of MML-1. Based on our work and previously published data we conclude that the internal proline-rich region of MML-1 is dispensable for DNA binding but is biologically important.