The NuRD complex component p66 suppresses photoreceptor neuron regeneration in planarians.
The NuRD complex component p66 suppresses photoreceptor neuron regeneration in planarians.
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DOI：
10.1002/reg2.58
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发表时间：
2016-06
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影响因子：
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通讯作者：
Petersen, Christian P
中科院分区：
文献类型：
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作者：
Vasquez-Doorman, Constanza;Petersen, Christian P
再生涉及精确控制细胞命运，以产生在芽基内形成的适当组织补充。一些染色质修饰复合物已被确定为在涡虫中再生所需的，但目前还不清楚这类分子是否均匀地促进分化细胞的产生。我们确定了p66的功能，编码NuRD（核小体重塑和脱乙酰基酶）复合物的DNA结合蛋白组分，以及染色体结构域解旋酶chd 4，在抑制光感受器神经元（PRN）的生产中。这种抑制作用似乎仅限于PRNs，因为p66抑制不影响眼色素杯细胞（PCCs）的数量，并减少脑神经元和表皮祖细胞的数量。来自p66（RNAi）动物的PRN分化有一些异常，但仍然产生向脑的抑制蛋白+投射。p66抑制产生过量的卵+otxA+ PRN祖细胞，而不影响卵+otxA-PCC祖细胞的数量，并且卵和otxA都是p66（RNAi）过量PRN表型所需的。总之，这些结果表明，p66通过NuRD复合物发挥作用，通过限制谱系特异性转录因子的表达来抑制PRN的产生。
Regeneration involves precise control of cell fate to produce an appropriate complement of tissues formed within a blastema. Several chromatin‐modifying complexes have been identified as required for regeneration in planarians, but it is unclear whether this class of molecules uniformly promotes the production of differentiated cells. We identify a function for p66, encoding a DNA‐binding protein component of the NuRD (nucleosome remodeling and deacetylase) complex, as well as the chromodomain helicase chd4, in suppressing production of photoreceptor neurons (PRNs) in planarians. This suppressive effect appeared restricted to PRNs because p66 inhibition did not influence numbers of eye pigment cup cells (PCCs) and decreased numbers of brain neurons and epidermal progenitors. PRNs from p66(RNAi) animals differentiated with some abnormalities but nonetheless produced arrestin+ projections to the brain. p66 inhibition produced excess ovo+otxA+ PRN progenitors without affecting numbers of ovo+otxA− PCC progenitors, and ovo and otxA were each required for the p66(RNAi) excess PRN phenotype. Together these results suggest that p66 acts through the NuRD complex to suppress PRN production by limiting expression of lineage‐specific transcription factors.