杆状裂变酵母通过两极和隔膜的细胞壁扩张生长,由必需的葡聚糖合酶合成。Bgs1在胞质分裂时合成初级隔膜的线性β(1,3)葡聚糖。线性β(1,3)葡聚糖也存在于壁极中,提示Bgs1在生长极性中的额外作用。我们的研究揭示了Bgs1和Tea1-Tea4之间的重要合作,但没有其他极性因素,控制生长极性。同时缺乏Bgs1功能和Tea1-Tea4会导致生长极性完全丧失,其他葡聚糖合酶的传播,和球形细胞的形成,表明这种缺陷是由于缺乏线性β(1,3)葡聚糖。此外,线性β(1,3)葡聚糖缺失诱导肌动蛋白斑块离域和固醇扩散,在没有Tea1-Tea4的情况下,它们最终导致生长极性损失。这表明Bgs1在胞质分裂和极化生长过程中控制肌动蛋白结构的功能具有很强的相似性。总的来说,我们的发现揭示了细胞壁β(1,3)葡聚糖调节极化生长,像神经元细胞中相当的细胞外基质。
Rod-shaped fission yeast grows through cell wall expansion at poles and septum, synthesized by essential glucan synthases. Bgs1 synthesizes the linear β(1,3)glucan of primary septum at cytokinesis. Linear β(1,3)glucan is also present in the wall poles, suggesting additional Bgs1 roles in growth polarity. Our study reveals an essential collaboration between Bgs1 and Tea1-Tea4, but not other polarity factors, in controlling growth polarity. Simultaneous absence of Bgs1 function and Tea1-Tea4 causes complete loss of growth polarity, spread of other glucan synthases, and spherical cell formation, indicating this defect is specifically due to linear β(1,3)glucan absence. Furthermore, linear β(1,3)glucan absence induces actin patches delocalization and sterols spread, which are ultimately responsible for the growth polarity loss without Tea1-Tea4. This suggests strong similarities in Bgs1 functions controlling actin structures during cytokinesis and polarized growth. Collectively, our findings unveil that cell wall β(1,3)glucan regulates polarized growth, like the equivalent extracellular matrix in neuronal cells.