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Effect of Water Stress on Cell Division and Cdc2-Like Cell Cycle Kinase Activity in Wheat Leaves

机译:水分胁迫对细胞分裂和Cdc2样细胞周期的影响 小麦叶片中的激酶活性

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摘要

In wheat (Triticum aestivum) seedlings subjected to a mild water stress (water potential of −0.3 MPa), the leaf-elongation rate was reduced by one-half and the mitotic activity of mesophyll cells was reduced to 42% of well-watered controls within 1 d. There was also a reduction in the length of the zone of mesophyll cell division to within 4 mm from the base compared with 8 mm in control leaves. However, the period of division continued longer in the stressed than in the control leaves, and the final cell number in the stressed leaves reached 85% of controls. Cyclin-dependent protein kinase enzymes that are required in vivo for DNA replication and mitosis were recovered from the meristematic zone of leaves by affinity for p13suc1. Water stress caused a reduction in H1 histone kinase activity to one-half of the control level, although amounts of the enzyme were unaffected. Reduced activity was correlated with an increased proportion of the 34-kD Cdc2-like kinase (an enzyme sharing with the Cdc2 protein of other eukaryotes the same size, antigenic sites, affinity for p13suc1, and H1 histone kinase catalytic activity) deactivated by tyrosine phosphorylation. Deactivation to 50% occurred within 3 h of stress imposition in cells at the base of the meristematic zone and was therefore too fast to be explained by a reduction in the rate at which cells reached mitosis because of slowing of growth; rather, stress must have acted more immediately on the enzyme. The operation of controls slowing the exit from the G1 and G2 phases is discussed. We suggest that a water-stress signal acts on Cdc2 kinase by increasing phosphorylation of tyrosine, causing a shift to the inhibited form and slowing cell production.
机译:在温和的水分胁迫下(水势为-0.3 MPa),小麦(Triticum aestivum)幼苗的叶片伸长率降低了一半,而叶肉细胞的有丝分裂活性则降低至灌溉良好的对照的42% 1 d内。与对照叶片的8 mm相比,叶肉细胞分裂区的长度也减少到距基部4 mm以内。但是,受胁迫叶片的分裂期比对照叶片更长,并且受胁迫叶片的最终细胞数达到了对照的85%。通过对p13 suc1 的亲和力从叶片的分生组织中回收了DNA复制和有丝分裂所需的细胞周期蛋白依赖性蛋白激酶。水分胁迫导致H1组蛋白激酶活性降低至对照水平的一半,尽管该酶的量不受影响。活性降低与34-kD Cdc2样激酶(与其他大小相同的真核生物的Cdc2蛋白共享的一种酶)的比例增加有关 位点,对p13 suc1 和H1组蛋白激酶的亲和力 催化活性)通过酪氨酸磷酸化而失活。 在施加压力后3小时内失活到50% 分生区底部的细胞,因此过快 用细胞到达率的降低来解释 由于生长减慢而导致的有丝分裂;相反,压力一定已经起作用 更直接地对酶。控件的操作减慢了 讨论了从G1和G2阶段退出。我们建议 水分胁迫信号通过增加磷酸化作用而作用于Cdc2激酶 酪氨酸,导致转移到抑制形式并减慢细胞 生产。

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