Nitric Oxide Mediates Cytokinin Functions in Cell Proliferation and Meristem Maintenance in Arabidopsis

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Abstract

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 nos1/noa1 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 nos1/noa1 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 confirmed by the genetic evidence that constitutive expression of CYCD3;1 complements the defects of nos1/noa1 mutant in meristematic activity in shoot, root, and floral tissues as well as in cytokinin-induced callus initiation and shoot regeneration. Furthermore, we show that NO deficiency caused by loss of NOS1/NOA1 impairs cellular development such as the duration of the mitotic phase and timing of the transition to endocycles in nos1/noa1 mutant leaves, which can be reverted by constitutive expression of CYCD3;1. Taken together, these results demonstrate that NO mediates transcriptional activation of CYCD3;1 in regulating the mitotic cycles in response to cytokinins.

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