Cytokinin and nitric oxide （NO） have been characterized as signaling molecules to trigger cell division in tissue culture. Here, we show that the hypocotyl and root explants of Arabidopsis NO-deficient mutant nosl/n...Cytokinin and nitric oxide （NO） have been characterized as signaling molecules to trigger cell division in tissue culture. Here, we show that the hypocotyl and root explants of Arabidopsis NO-deficient mutant nosl/noal exhibit severe defects in callus induction and shoot regeneration in response to cytokinin. Accordingly, depletion of NO caused by a NO scavenger leads to a severe inhibitory effect on callus induction. Moreover, cytokinin-induced NO production is impaired in nosl/noal in which cytokinin-triggered activation of cell cycle gene CYCD3;1 is inhibited, indicating that NO may act downstream of cytokinin in the control of cell proliferation through CYCD3;1. This hypothesis is further con- firmed by the genetic evidence that constitutive expression of CYCD3;1 complements the defects of nosl/noal mutant in meristematic activity in shoot, root, and floral tissues as well as in cytokinin-induced callus initiation and shoot regen- eration. Furthermore, we show that NO deficiency caused by loss of NOSl/NOA1 impairs cellular development such as the duration of the mitotic phase and timing of the transition to endocycles in nosl/noal mutant leaves, which can be reverted by constitutive expression of CYCD3;1. Taken together, these results demonstrate that NO mediates transcrip- tional activation of CYCD3,1 in regulating the mitotic cycles in response to cytokinins.展开更多
基金This research was supported in parts by the Ministry of Science and Technology of China，the Ministry of Agriculture of China，the National Natural Science Foundation of China，the CAS/SAFEA International Partnership Program for Creative Research Teams
文摘Cytokinin and nitric oxide （NO） have been characterized as signaling molecules to trigger cell division in tissue culture. Here, we show that the hypocotyl and root explants of Arabidopsis NO-deficient mutant nosl/noal exhibit severe defects in callus induction and shoot regeneration in response to cytokinin. Accordingly, depletion of NO caused by a NO scavenger leads to a severe inhibitory effect on callus induction. Moreover, cytokinin-induced NO production is impaired in nosl/noal in which cytokinin-triggered activation of cell cycle gene CYCD3;1 is inhibited, indicating that NO may act downstream of cytokinin in the control of cell proliferation through CYCD3;1. This hypothesis is further con- firmed by the genetic evidence that constitutive expression of CYCD3;1 complements the defects of nosl/noal mutant in meristematic activity in shoot, root, and floral tissues as well as in cytokinin-induced callus initiation and shoot regen- eration. Furthermore, we show that NO deficiency caused by loss of NOSl/NOA1 impairs cellular development such as the duration of the mitotic phase and timing of the transition to endocycles in nosl/noal mutant leaves, which can be reverted by constitutive expression of CYCD3;1. Taken together, these results demonstrate that NO mediates transcrip- tional activation of CYCD3,1 in regulating the mitotic cycles in response to cytokinins.
