|WANG, DALI - Zhejiang University|
|SHI, YA-FEI - Zhejiang University|
|WANG, CHAO - Zhejiang University|
|COHEN, JERRY - University Of Minnesota|
|HENDRICKSON CULLER, ANGELA - Monsanto Corporation|
|LIU, JIAN-ZHONG - Zhejiang University|
Submitted to: Molecular Plant
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/31/2014
Publication Date: N/A
Interpretive Summary: Crosstalk between phytohormones nitric oxide and auxin is medicated by S-nitrosylation, which regulates auxin signaling and transport and Arabidopsis growth and development.
Technical Abstract: Nitric oxide (NO) and auxin phytohormone cross talk has been implicated in plant development and growth. Addition and removal of NO moieties to cysteine residues of proteins, is termed S-nitrosylation and de-nitrosylation, respectively and functions as an on/off switch of protein activity. This dynamic process has been suggested to mediate NO-auxin cross talk by altering the activity of proteins required for auxin processes. De-nitrosylation is catalyzed by S-nitrosoglutathione reductase (GSNOR) and in the Arabidopsis GSNOR loss of function mutant, gsnor1-3, higher levels of S-nitrosylated proteins accumulate and plants display several developmental defects similar to those with impaired auxin signaling and auxin transport. Recent studies indicate that impaired de-nitrosylation affects proteins required for either auxin transport or auxin signaling however, the potential broader role of S-nitrosylation in mediating NO-auxin cross talk and development remains unresolved. In this study we used a genetic approach to understand the broader role of S-nitrosylation in auxin signaling and auxin transport in Arabidopsis growth and development. Our results showed that although auxin levels are similar in wild type and gsnor1-3 and similar in tissues at different developmental times, both auxin signaling and polar auxin transport are compromised in gsnor1-3. Our results suggest that S-nitrosylation and GSNOR-mediated de-nitrosylation mediate NO-auxin cross talk and auxin homeostasis by regulating the activity of different proteins in both auxin signaling and in auxin transport.