Downloads and Tools

•  Article PDF
  670.27 KB PDF document

This is an open access article.
Print this page Email this page

Recipient's Email:

---

Article Citation

RIS
MARC (XML)
FULL CITATION (TXT)

---

Share on Facebook

Authors: Wei Ma and Gerald A. Berkowitz

Wei Ma

Corresponding author: mawei@msu.edu
Department of Energy Plant Research Laboratory, Michigan State University, East Lansing, MI USA

Gerald A. Berkowitz

Agricultural Biotechnology Laboratory, Department of Plant Science, University of Connecticut, Storrs, CT USA

Abstract:

Previous studies reveal that both Ca²⁺ and nitric oxide (NO) play pivotal roles in the plant senescence signaling cascade. However, not much is known about the molecular identity of the Ca²⁺ entry during senescence programming and its relationship to the downstream NO signal. Our recent study shows that Arabidopsis cyclic nucleotide gated channel2 (CNGC2) contributes to Ca²⁺ uptake and senescence signaling. The CNGC2 loss-of-function mutant dnd1 displays reduced Ca²⁺ accumulation in leaves and a series of early senescence phenotypes compared to wild type (WT). Notably, endogenous NO content in dnd1 leaves is lower than leaves of WT. Application of an NO donor can effectively rescue a number of early senescence phenotypes found in the dnd1 plants. Current evidence supports the notion that NO functions as a negative regulator in senescence signaling and our model supports this point. In this article, we expand our discussion of CNGC2 mediated Ca²⁺ uptake and other related signaling components involved in the plant senescence signaling cascade.

Article Addendum to:
W Ma, A Smigel, RK Walker, W Moeder, K Yoshioka, GA Berkowitz. Leaf senescence signaling: the Ca2+-conducting Arabidopsis cyclic nucleotide gated channel2 acts through nitric oxide to repress senescence programming. Plant Physiol 2010; 154: 733-43
PMID: 20699402 DOI: 10.1104/pp.110.16135

Received: December 2, 2010; Accepted: December 2, 2010

Preview: