Stephenson Karen S, Gow Neil A R, Davidson Fordyce A, Gadd Geoffrey M
Division of Molecular Microbiology, College of Life Sciences, University of Dundee, Dundee, DD1 5EH Scotland, United Kingdom.
The Aberdeen Fungal Group, School of Medical Sciences, Institute of Medical, Sciences, University of Aberdeen, Aberdeen, AB25 2ZD Scotland, United Kingdom.
Fungal Biol. 2014 Mar;118(3):287-94. doi: 10.1016/j.funbio.2013.12.007. Epub 2014 Jan 4.
Thigmotropism is the ability of an organism to respond to a topographical stimulus by altering its axis of growth. The thigmotropic response of the model fungus Neurospora crassa was quantified using microfabricated glass slides with ridges of defined height. We show that the polarity machinery at the hyphal tip plays a role in the thigmotropic response of N. crassa. Deletion of N. crassa genes encoding the formin, BNI-1, and the Rho-GTPase, CDC-42, an activator of BNI-1 in yeast, CDC-24, its guanine nucleotide exchange factor (GEF), and BEM-1, a scaffold protein in the same pathway, were all shown to significantly decrease the thigmotropic response. In contrast, deletion of genes encoding the cell end-marker protein, TEA-1, and KIP-1, the kinesin responsible for the localisation of TEA-1, significantly increased the thigmotropic response. These results suggest a mechanism of thigmotropism involving vesicle delivery to the hyphal tip via the actin cytoskeleton and microtubules. Neurospora crassa thigmotropic response differed subtly from that of Candida albicans where the stretch-activated calcium channel, Mid1, has been linked with thigmotropic behaviour. The MID-1 deficient mutant of N. crassa (Δmid-1) and the effects of calcium depletion were examined here but no change in the thigmotropic response was observed. However, SPRAY, a putative calcium channel protein, was shown to be required for N. crassa thigmotropism. We propose that the thigmotropic response is a result of changes in the polarity machinery at the hyphal tip which are thought to be downstream effects of calcium signalling pathways triggered by mechanical stress at the tip.
向触性是生物体通过改变其生长轴来响应地形刺激的能力。使用具有确定高度脊的微加工载玻片对模式真菌粗糙脉孢菌的向触性反应进行了量化。我们表明，菌丝尖端的极性机制在粗糙脉孢菌的向触性反应中起作用。编码formin（BNI-1）和Rho-GTPase（CDC-42，酵母中BNI-1的激活剂）、其鸟嘌呤核苷酸交换因子（GEF）CDC-24以及同一途径中的支架蛋白BEM-1的粗糙脉孢菌基因的缺失，均显示出显著降低向触性反应。相反，编码细胞末端标记蛋白TEA-1和负责TEA-1定位的驱动蛋白KIP-1的基因缺失，显著增加了向触性反应。这些结果表明了一种向触性机制，涉及通过肌动蛋白细胞骨架和微管将囊泡递送至菌丝尖端。粗糙脉孢菌的向触性反应与白色念珠菌的向触性反应略有不同，在白色念珠菌中，拉伸激活的钙通道Mid1与向触性行为有关。本文研究了粗糙脉孢菌的MID-1缺陷突变体（Δmid-1）和钙耗竭的影响，但未观察到向触性反应的变化。然而，一种假定的钙通道蛋白SPRAY被证明是粗糙脉孢菌向触性所必需的。我们提出，向触性反应是菌丝尖端极性机制变化的结果，这些变化被认为是由尖端机械应力触发的钙信号通路的下游效应。
