Schuppler U, He PH, John PC, Munns R
Plant Physiol. 1998 Jun;117(2):667-78. doi: 10.1104/pp.117.2.667.
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 p13(suc1). 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 p13(suc1), 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.
在遭受轻度水分胁迫（水势为-0.3 MPa）的小麦（普通小麦）幼苗中，叶片伸长速率降低了一半，叶肉细胞的有丝分裂活性在1天内降至充分浇水对照的42%。与对照叶片中8毫米相比，叶肉细胞分裂区的长度也缩短至距基部4毫米以内。然而，胁迫叶片中的分裂期持续时间比对照叶片更长，胁迫叶片中的最终细胞数量达到对照的85%。通过对p13(suc1)的亲和力，从叶片的分生组织区中回收了体内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，尽管该酶的量未受影响。活性降低与通过酪氨酸磷酸化失活的34-kD Cdc2样激酶（一种与其他真核生物的Cdc2蛋白具有相同大小、抗原位点、对p13(suc1)的亲和力和H1组蛋白激酶催化活性的酶）比例增加相关。在分生组织区基部的细胞中，胁迫施加后3小时内失活至50%，因此太快而无法用由于生长减慢导致细胞进入有丝分裂的速率降低来解释；相反，胁迫一定是更直接地作用于该酶。讨论了控制G1和G2期退出减慢的机制。我们认为水分胁迫信号通过增加酪氨酸磷酸化作用于Cdc2激酶，导致转变为抑制形式并减慢细胞产生。
