Salt stress affects cortical microtubule organization and helical growth in Arabidopsis.
Salt stress affects cortical microtubule organization and helical growth in Arabidopsis.
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DOI：
10.1093/pcp/pcj090
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发表时间：
2006-08
影响因子：
4.9
通讯作者：
T. Shoji;Koya Suzuki;Tatsuya Abe;Y. Kaneko;Huazhong Shi;Jian‐Kang Zhu;A. Rus;P. Hasegawa;T. Hashimoto
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文献类型：
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作者：
T. Shoji;Koya Suzuki;Tatsuya Abe;Y. Kaneko;Huazhong Shi;Jian‐Kang Zhu;A. Rus;P. Hasegawa;T. Hashimoto
皮层微管阵列在决定植物细胞的生长轴方面是至关重要的，并且已知各种环境和生理因素会影响阵列组织。微管组织的spiral 1突变体拟南芥，它显示了右手螺旋生长表型在迅速伸长的表皮细胞部分中断。我们发现，质膜Na（+）/H（+）反向转运蛋白SOS 1及其调节激酶SOS 2的突变有效地抑制了spiral 1的微管破坏和螺旋生长表型，并且在没有盐胁迫的情况下，sos 1和sos 2根对低剂量微管相互作用药物的螺旋生长反应发生了改变。盐胁迫也改变了野生型根对药物的生长反应。螺旋生长的抑制似乎是特定于spiral 1，因为其他螺旋生长突变体没有获救。sos 1在抑制spiral 1缺陷和引起异常药物反应中的作用在根中hkt 1 Na（+）内流载体突变的存在下被抵消，但在下胚轴中没有。这些结果表明，细胞质的盐不平衡所造成的不足SOS 1活性损害皮质微管功能，其中微管定位SPIRAL 1是专门参与。
Cortical microtubule arrays are critical in determining the growth axis of diffusely growing plant cells, and various environmental and physiological factors are known to affect the array organization. Microtubule organization is partly disrupted in the spiral1 mutant of Arabidopsis thaliana, which displays a right-handed helical growth phenotype in rapidly elongating epidermal cells. We show here that mutations in the plasma membrane Na(+)/H(+) antiporter SOS1 and its regulatory kinase SOS2 efficiently suppressed both microtubule disruption and helical growth phenotypes of spiral1, and that sos1 and sos2 roots in the absence of salt stress exhibited altered helical growth response to microtubule-interacting drugs at low doses. Salt stress also altered root growth response to the drugs in wild-type roots. Suppression of helical growth appeared to be specific to spiral1 since other helical growth mutants were not rescued. The effects of sos1 in suppressing spiral1 defects and in causing abnormal drug responses were nullified in the presence of the hkt1 Na(+) influx carrier mutation in roots but not in hypocotyls. These results suggest that cytoplasmic salt imbalance caused by insufficient SOS1 activity compromises cortical microtubule functions in which microtubule-localized SPIRAL1 is specifically involved.