Please use this identifier to cite or link to this item: http://223.31.159.10:8080/jspui/handle/123456789/803
Title: Arabidopsis RSS1 mediates cross-talk between glucose and light signaling during hypocotyl elongation growth
Authors: Singh, Manjul
Gupta, Aditi
Singh, Dhriti
Khurana, Jitendra P.
Laxmi, Ashverya
Keywords: Plant signalling
Plant physiology
Arabidopsis
Light Signaling
Glucose
RSS1 Mediates Cross-Talk
Issue Date: 2017
Publisher: Nature Publishing Group
Citation: Scientific Reports, 7(1): 16101
Abstract: Plants possess exuberant plasticity that facilitates its ability to adapt and survive under challenging environmental conditions. The developmental plasticity largely depends upon cellular elongation which is governed by a complex network of environmental and phytohormonal signals. Here, we report role of glucose (Glc) and Glc-regulated factors in controlling elongation growth and shade response in Arabidopsis. Glc controls shade induced hypocotyl elongation in a dose dependent manner. We have identified a Glc repressed factor REGULATED BY SUGAR AND SHADE1 (RSS1) encoding for an atypical basic helix-loop-helix (bHLH) protein of unknown biological function that is required for normal Glc actions. Phenotype analysis of mutant and overexpression lines suggested RSS1 to be a negative regulator of elongation growth. RSS1 affects overall auxin homeostasis. RSS1 interacts with the elongation growth-promoting proteins HOMOLOG OF BEE2 INTERACTING WITH IBH 1 (HBI1) and BR ENHANCED EXPRESSION2 (BEE2) and negatively affects the transcription of their downstream targets such as YUCs, INDOLE-3-ACETIC ACID INDUCIBLE (IAAs), LONG HYPOCOTYL IN FAR-RED1 (HFR1), HOMEOBOX PROTEIN 2 (ATHB2), XYLOGLUCAN ENDOTRANSGLUCOSYLASE/HYDROLASES (XTHs) and EXPANSINS. We propose, Glc signals might maintain optimal hypocotyl elongation under multiple signals such as light, shade and phytohormones through the central growth regulatory bHLH/HLH module.
Description: Accepted date: 09 November 2017
URI: http://223.31.159.10:8080/jspui/handle/123456789/803
ISSN: 2045-2322
Appears in Collections:Institutional Publications

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