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Myosin-5 kinesin-1 and myosin-17 cooperate in secretion of fungal chitin synthase

机译:Myosin-5kinesin-1和myosin-17协同分泌真菌几丁质合酶

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摘要

Plant infection by pathogenic fungi requires polarized secretion of enzymes, but little is known about the delivery pathways. Here, we investigate the secretion of cell wall-forming chitin synthases (CHSs) in the corn pathogen Ustilago maydis. We show that peripheral filamentous actin (F-actin) and central microtubules (MTs) form independent tracks for CHSs delivery and both cooperate in cell morphogenesis. The enzyme Mcs1, a CHS that contains a myosin-17 motor domain, is travelling along both MTs and F-actin. This transport is independent of kinesin-3, but mediated by kinesin-1 and myosin-5. Arriving vesicles pause beneath the plasma membrane, but only ∼15% of them get exocytosed and the majority is returned to the cell centre by the motor dynein. Successful exocytosis at the cell tip and, to a lesser extent at the lateral parts of the cell requires the motor domain of Mcs1, which captures and tethers the vesicles prior to secretion. Consistently, Mcs1-bound vesicles transiently bind F-actin but show no motility in vitro. Thus, kinesin-1, myosin-5 and dynein mediate bi-directional motility, whereas myosin-17 introduces a symmetry break that allows polarized secretion.
机译:病原真菌对植物的感染需要酶的极化分泌,但对于传递途径知之甚少。在这里,我们调查玉米病原体Ustilago maydis中细胞壁形成几丁质合酶(CHSs)的分泌。我们显示,外周丝状肌动蛋白(F-肌动蛋白)和中央微管(MTs)形成CHSs传递独立的轨道,并且两者都在细胞形态发生中合作。 CHS包含肌球蛋白17运动域的CHS酶Mcs1沿着MT和F-肌动蛋白移动。这种运输独立于驱动蛋白3,但由驱动蛋白1和肌球蛋白5介导。到达的囊泡停在质膜下,但只有约15%的囊泡被胞吐,大部分通过动力动力蛋白返回到细胞中心。要想在细胞末端成功地进行胞吐作用,在较小程度上在细胞的外侧部分就需要胞外域Mcs1,该域可以在分泌前捕获并束缚囊泡。一致地,与Mcs1结合的囊泡暂时结合F-肌动蛋白,但在体外没有运动性。因此,kinesin-1,myosin-5和dynein介导双向运动,而myosin-17引入了对称断裂,允许极化分泌。

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