Please use this identifier to cite or link to this item: http://223.31.159.10:8080/jspui/handle/123456789/340
Title: The interaction between glucose and cytokinin signal transduction pathway in Arabidopsis thaliana
Authors: Kushwah, Sunita
Laxmi, Ashverya
Keywords: hypocotyl
microarray
signalling
sugar
Issue Date: 2013
Publisher: John Wiley & Sons
Citation: Plant Cell and Environment, 37(1): 235-253
Abstract: Cytokinins (CKs) and glucose (GLC) control a number of common responses in plants. We hypothesize that there may be an extensive overlap between CK- and GLC-signalling pathways. Microarray along with physiological analysis has been performed to find out the interdependence/overlap between CK and GLC signal transduction pathways in Arabidopsis seedlings. GLC could transcriptionally affect 76% of CK-regulated genes at whole genome level, 89% of which are agonistically regulated. GLC may also affect CK-regulated gene expression via non-transcriptional pathways. GLC can regulate several genes involved in CK metabolism and signalling. A number of gene families involved in development and stress are commonly regulated by CK and GLC. Physiologically, both GLC and CK could regulate hypocotyl length in dark. GLC and CK signalling may integrate at the level of type A Arabidopsis response regulators (ARRs) in controlling hypocotyl length. Both GLC and CK signalling cannot alter hypocotyl length in dark in auxin-signalling mutants auxin response2/indole-3-acetic acid7 (AXR2/IAA7) and AXR3/IAA17 suggesting that they may involve auxin-signalling component as a nodal point. Here, we demonstrate that there is an extensive overlap between CK- and GLC-regulated gene expression and physiological responses.
Description: Accepted date: 20 May 2013
URI: http://172.16.0.77:8080/jspui/handle/123456789/340
ISSN: 0140-7791
Appears in Collections:Institutional Publications

Files in This Item:
File Description SizeFormat 
Laxmi A_2013_1.pdf
  Restricted Access
1.1 MBAdobe PDFView/Open Request a copy


Items in IR@NIPGR are protected by copyright, with all rights reserved, unless otherwise indicated.