Howard Hughes Medical Institute and Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
PLoS Genet. 2012;8(10):e1003004. doi: 10.1371/journal.pgen.1003004. Epub 2012 Oct 18.
The rod-shaped fission yeast Schizosaccharomyces pombe, which undergoes cycles of monopolar-to-bipolar tip growth, is an attractive organism for studying cell-cycle regulation of polarity establishment. While previous research has described factors mediating this process from interphase cell tips, we found that division site signaling also impacts the re-establishment of bipolar cell growth in the ensuing cell cycle. Complete loss or targeted disruption of the non-essential cytokinesis protein Fic1 at the division site, but not at interphase cell tips, resulted in many cells failing to grow at new ends created by cell division. This appeared due to faulty disassembly and abnormal persistence of the cell division machinery at new ends of fic1Δ cells. Moreover, additional mutants defective in the final stages of cytokinesis exhibited analogous growth polarity defects, supporting that robust completion of cell division contributes to new end-growth competency. To test this model, we genetically manipulated S. pombe cells to undergo new end take-off immediately after cell division. Intriguingly, such cells elongated constitutively at new ends unless cytokinesis was perturbed. Thus, cell division imposes constraints that partially override positive controls on growth. We posit that such constraints facilitate invasive fungal growth, as cytokinesis mutants displaying bipolar growth defects formed numerous pseudohyphae. Collectively, these data highlight a role for previous cell cycles in defining a cell's capacity to polarize at specific sites, and they additionally provide insight into how a unicellular yeast can transition into a quasi-multicellular state.
杆状裂殖酵母 Schizosaccharomyces pombe 经历从单极到两极尖端生长的循环,是研究细胞周期极性建立调控的理想生物体。虽然之前的研究已经描述了从中期细胞尖端调节这个过程的因素,但我们发现分裂位点信号也会影响下一个细胞周期中两极细胞生长的重新建立。在分裂位点完全缺失或靶向破坏非必需的胞质分裂蛋白 Fic1,但不在中期细胞尖端,导致许多细胞无法在细胞分裂产生的新末端生长。这似乎是由于 fic1Δ 细胞新末端的细胞分裂机制的错误组装和异常持续存在。此外,在胞质分裂最后阶段有缺陷的其他突变体表现出类似的生长极性缺陷,支持细胞分裂的强大完成有助于新末端生长能力。为了验证这个模型,我们通过遗传操作使 S. pombe 细胞在细胞分裂后立即进行新末端起始。有趣的是,除非胞质分裂受到干扰,否则这些细胞会在新末端持续伸长。因此,细胞分裂施加了限制,部分覆盖了生长的正向控制。我们假设这种限制有助于侵袭性真菌的生长,因为表现出两极生长缺陷的胞质分裂突变体形成了许多假菌丝。总的来说,这些数据突出了前一个细胞周期在确定细胞在特定部位极化的能力方面的作用,并且它们还提供了关于单细胞酵母如何过渡到准多细胞状态的见解。