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ARS Home » Pacific West Area » Albany, California » Plant Gene Expression Center » Research » Publications at this Location » Publication #320125
Title: Loss of GSNOR1 function leads to compromised auxin signaling and polar auxin transport

Author
item WANG, DALI - Zhejiang University
item SHI, YA-FEI - Zhejiang University
item WANG, CHAO - Zhejiang University
item COHEN, JERRY - University Of Minnesota
item HENDRICKSON CULLER,, ANGELA - University Of Minnesota
item Baker, Barbara
item LIU, JIAN-ZHONG - Zhejiang University

Submitted to: Molecular Plant
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/16/2015
Publication Date: 4/23/2015
Publication URL: http://dx.doi.org/10.1016/j.molp.2015.04.008
Citation: Wang, D., Shi, Y., Wang, C., Cohen, J., Hendrickson Culler, A., Baker, B.J., Liu, J. 2015. Loss of GSNOR1 function leads to compromised auxin signaling and polar auxin transport. Molecular Plant. 8(9):1350-1365.

Interpretive Summary: The plant hormone auxin is responsible for many aspects of plant biology. One of the mechanisms by which auxin is thought to have an effect is by altering the activity of proteins required for auxin processes through the addition or removal of nitric oxide (NO) to proteins. The gene that takes off NO is GSNOR and mutants in this gene display several developmental defects similar to those with impaired auxin signaling and auxin transport. This studies shows that both auxin signaling and polar auxin transport are compromised in gsnor1-3 compared to wild type although auxin levels are similar in both. The results provide a mechanistic understanding into the broad role of auxin in plant biology.

Technical Abstract: Nitric oxide (NO) and auxin phytohormone cross talk has been implicated in plant development and growth. Addition and removal of NO 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 as a mediator of 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 both auxin signaling and polar auxin transport are compromised in gsnor1-3 compared to wild type although auxin levels are similar in both. 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.