Cold stress response in Arabidopsis thaliana is mediated by GNOM ARF-GEF.

Endosomal trafficking plays an important role in regulating plant growth and development both at optimal and stressed conditions. Cold stress response in Arabidopsis root is directly linked to inhibition of the endosomal trafficking of auxin efflux carriers. However, the cellular components that link cold stress and the endosomal trafficking remain elusive. By screening available endosomal trafficking mutants against root growth recovery response under cold stress, we identified GNOM, a SEC7 containing ARF-GEF, as a major modulator of cold response. Contrasting response of partial loss of function mutant gnom^{B4049/emb30-1} and the engineered Brefeldin A (BFA)-resistant GNOM line, both of which contain mutations within SEC7 domain, to cold stress at the whole-plant level highlights the importance of this domain in modulating the cold response pathway of plants. Cold stress selectively and transiently inhibits GNOM expression. The engineered point mutation at 696 amino acid position (Methionine to Leucine) that makes GNOM resistant to BFA in fact results in overexpression of GNOM both at transcriptional and translational levels, and also alters its subcellular localization. Overexpression and altered cellular localization of GNOM were found to be directly linked to conferring striking cold-resistant phenotype in Arabidopsis. Collectively, these results provide a mechanistic link between GNOM, BFA-sensitive GNOM-regulated trafficking and cold stress.

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