Abstract：
Spatial periodic signal for cell differentiation in some multicellular organisms is generated according to Turing\'s principle for pattern formation. How a dividing cell responds to the signal of differentiation is addressed with the filamentous cyanobacterium Nostoc sp. PCC 7120, which forms the patterned distribution of heterocysts. We show that differentiation of a dividing cell was delayed until its division was completed and only one daughter cell became heterocyst. A mutant of patU3, which encodes an inhibitor of heterocyst formation, showed no such delay and formed heterocyst pairs from the daughter cells of cell division or dumbbell-shaped heterocysts from the cells undergoing cytokinesis. The patA mutant, which forms heterocysts only at the filament ends, restored intercalary heterocysts by a single nucleotide mutation of patU3, and double mutants of patU3/patA and patU3/hetF had the phenotypes of the patU3 mutant. We provide evidence that HetF, which can degrade PatU3, is recruited to cell divisome through its C-terminal domain. A HetF mutant with its N-terminal peptidase domain but lacking the C-terminal domain could not prevent the formation of heterocyst pairs, suggesting that the divisome recruitment of HetF is needed to sequester HetF for the delay of differentiation in dividing cells. Our study demonstrates that PatU3 plays a key role in cell-division coupled control of differentiation.
摘要：
一些多细胞生物中细胞分化的空间周期信号是根据图灵模式形成原理产生的。用丝状蓝细菌Nostocsp解决了分裂细胞如何响应分化信号。PCC7120，形成杂环的图案化分布。我们表明，分裂细胞的分化被延迟，直到其分裂完成，只有一个子细胞成为异形细胞。patU3的突变体，它编码异形形成的抑制剂，没有显示出这种延迟，并且从细胞分裂的子细胞中形成了异形对，或者从进行胞质分裂的细胞中形成了哑铃形异形。patA突变体,仅在细丝末端形成杂环，patU3的单核苷酸突变恢复了cal间杂环，patU3/patA和patU3/hetF的双突变体具有patU3突变体的表型。我们提供的证据表明HetF,可以降解PatU3的细胞通过其C末端结构域被募集到细胞分裂体。具有N末端肽酶结构域但缺乏C末端结构域的HetF突变体不能阻止杂环对的形成，这表明需要HetF的分裂体募集来隔离HetF，以延迟分裂细胞的分化。我们的研究表明，PatU3在分化的细胞分裂耦合控制中起着关键作用。
