CulB, a putative ubiquitin ligase subunit, regulates prestalk cell differentiation and morphogenesis in Dictyostelium spp.
CulB, a putative ubiquitin ligase subunit, regulates prestalk cell differentiation and morphogenesis in Dictyostelium spp.
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CulB 是一种假定的泛素连接酶亚基，可调节盘基网柄菌属的前茎细胞分化和形态发生。
DOI：
10.1128/ec.1.1.126-136.2002
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Kuspa,Adam
中科院分区：
文献类型：
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作者：
Wang,Bin;Kuspa,Adam
Dictyosteliumamoebae通过聚集成一个小丘，形成一个具有终末分化孢子和柄细胞的单一子实体来完成饥饿诱导的发育过程。culb被鉴定为在一个具有异常柄前细胞分化表型的发育突变中被破坏的基因。culbgene产物似乎是cullin蛋白家族的同源物，cullin蛋白家族已知参与泛素介导的蛋白质降解。突变体在每个正在发育的小丘上形成多余的茎尖，从而形成多个小子实体。茎前特异性基因表达了早熟的诱导突变体，表明茎前细胞分化比正常情况发生得更早。此外，当ulb突变细胞与野生型细胞混合时，它们表现出细胞自主形成茎细胞的倾向。因此，CulB似乎确保了在发育过程中适当的时间有适当数量的前柄细胞分化。通过破坏调控亚基基因（pkaR）或过表达催化亚基基因（pkaC）激活环amp依赖性蛋白激酶（PKA），可增强culb突变体的茎前/茎细胞分化表型。例如，culB - pkaR -细胞形成茎细胞，没有明显的多细胞形态发生，并且对茎前O （pstO）细胞诱导剂DIF-1更敏感。PKA激活的致敏条件表明，CulB可能通过控制细胞对DIF-1的敏感性来调控前柄细胞分化inDictyostelium，可能通过调节前柄分化速率限制的一种或多种蛋白的水平。
Dictyosteliumamoebae accomplish a starvation-induced developmental process by aggregating into a mound and forming a single fruiting body with terminally differentiated spores and stalk cells.culBwas identified as the gene disrupted in a developmental mutant with an aberrant prestalk cell differentiation phenotype. TheculBgene product appears to be a homolog of the cullin family of proteins that are known to be involved in ubiquitin-mediated protein degradation. TheculBmutants form supernumerary prestalk tips atop each developing mound that result in the formation of multiple small fruiting bodies. The prestalk-specific geneecmAis expressed precociously inculBmutants, suggesting that prestalk cell differentiation occurs earlier than normal. In addition, whenculBmutant cells are mixed with wild-type cells, they display a cell-autonomous propensity to form stalk cells. Thus, CulB appears to ensure that the proper number of prestalk cells differentiate at the appropriate time in development. Activation of cyclic AMP-dependent protein kinase (PKA) by disruption of the regulatory subunit gene (pkaR) or by overexpression of the catalytic subunit gene (pkaC) enhances the prestalk/stalk cell differentiation phenotype of theculBmutant. For example,culB−pkaR−cells form stalk cells without obvious multicellular morphogenesis and are more sensitive to the prestalk O (pstO) cell inducer DIF-1. The sensitized condition of PKA activation reveals that CulB may govern prestalk cell differentiation inDictyostelium, in part by controlling the sensitivity of cells to DIF-1, possibly by regulating the levels of one or more proteins that are rate limiting for prestalk differentiation.