Polarized morphogenesis is achieved by targeting or inhibiting growth at distinct regions. Rod-shaped fission yeast cells grow exclusively at their ends by restricting exocytosis and secretion to these sites. This growth pattern implies the existence of mechanisms that prevent exocytosis and growth along non-growing cell sides. We previously identified a set of 50-100 megadalton-sized node structures along the sides of fission yeast cells that contain the interacting proteins Skb1 and Slf1. Here, we show that Skb1-Slf1 nodes contain the syntaxin-like SNARE Psy1, which mediates exocytosis in fission yeast. Psy1 localizes in a diffuse pattern at cell tips where it likely promotes exocytosis and growth, but Psy1 is sequestered in Skb1-Slf1 nodes at cell sides where growth does not occur. Mutations that prevent node assembly or inhibit Psy1 localization to nodes lead to aberrant exocytosis at cell sides and increased cell width. Genetic results indicate that this Psy1 node mechanism acts in parallel to actin cables and Cdc42 regulation. Our work suggests that sequestration of syntaxin-like Psy1 at non-growing regions of the cell cortex reinforces cell morphology by restricting exocytosis to proper sites of polarized growth.

极化形态发生是通过靶向或抑制不同区域的生长来实现的。杆状裂殖酵母细胞通过限制胞吐作用和分泌到这些位点，仅在其末端生长。这种生长模式意味着存在阻止胞吐作用和沿非生长细胞侧面生长的机制。我们之前在裂殖酵母细胞的侧面鉴定了一组 50-100 兆道尔顿大小的节点结构，其中包含相互作用的蛋白质 Skb1 和 Slf1。在这里，我们发现 Skb1-Slf1 节点包含类似突触融合蛋白的 SNARE Psy1，它介导裂殖酵母中的胞吐作用。Psy1 以扩散模式定位在细胞尖端，可能促进胞吐作用和生长，但 Psy1 被隔离在不发生生长的细胞侧的 Skb1-Slf1 节点中。阻止节点组装或抑制 Psy1 定位到节点的突变会导致细胞侧的异常胞吐作用和细胞宽度增加。遗传结果表明，这种 Psy1 节点机制与肌动蛋白电缆和 Cdc42 调节并行作用。我们的工作表明，在细胞皮层的非生长区域隔离类突触蛋白 Psy1 通过将胞吐作用限制在极化生长的适当位点来增强细胞形态。