TY - JOUR
T1 - Signaling pathways mediating the suppression of Arabidopsis thaliana Ku gene expression by abscisic acid
AU - Liu, Pei Feng
AU - Chang, Wen Chi
AU - Wang, Yung Kai
AU - Chang, Hwan You
AU - Pan, Rong Long
N1 - Funding Information:
The authors would like to thank the National Science Council of the Republic of China, Taiwan, for financially supporting this research (NSC90-2311-B-007-B30, NSC91-2311-B-007-034, NSC95-2311-B-007-004) to R.L.P. We sincerely appreciate Dr. Wei-Yuan Chow and Dr. Shu-Hsing Wu for their technique assistance and suggestions during the course of this work.
PY - 2008/3
Y1 - 2008/3
N2 - The Ku heterodimer facilitates the regulation of DNA repair, DNA replication, cell cycle, and telomere maintenance. The plant hormone abscisic acid (ABA) is a plant growth inhibitor. This study investigates how Arabidopsis thaliana Ku (AtKu) genes are regulated by ABA in 3-week-old seedlings. First, β-Glucuronidase assay and real time quantitative PCR analysis results indicate that ABA represses the AtKu gene in a time- and concentration-dependent manner. However, adding of ABA biosynthesis inhibitors, fluride and tungate, did not eliminate AtKu suppression. Moreover, analysis of inhibitor treatments and ABA-responsive mutants suggested that AtKu repression by ABA was mediated through the pathway of extracellular Ca2+, phospholipase D alpha, p38-type mitogen-activated protein kinase (MAPK), MAPK6 and ABA transcription factors, ABI3 and ABI5. Finally, no cross-talk in modulating AtKu gene expression existed between ABA and antagonist hormones (auxins and gibberellic acid).
AB - The Ku heterodimer facilitates the regulation of DNA repair, DNA replication, cell cycle, and telomere maintenance. The plant hormone abscisic acid (ABA) is a plant growth inhibitor. This study investigates how Arabidopsis thaliana Ku (AtKu) genes are regulated by ABA in 3-week-old seedlings. First, β-Glucuronidase assay and real time quantitative PCR analysis results indicate that ABA represses the AtKu gene in a time- and concentration-dependent manner. However, adding of ABA biosynthesis inhibitors, fluride and tungate, did not eliminate AtKu suppression. Moreover, analysis of inhibitor treatments and ABA-responsive mutants suggested that AtKu repression by ABA was mediated through the pathway of extracellular Ca2+, phospholipase D alpha, p38-type mitogen-activated protein kinase (MAPK), MAPK6 and ABA transcription factors, ABI3 and ABI5. Finally, no cross-talk in modulating AtKu gene expression existed between ABA and antagonist hormones (auxins and gibberellic acid).
UR - http://www.scopus.com/inward/record.url?scp=40749100211&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=40749100211&partnerID=8YFLogxK
U2 - 10.1016/j.bbagrm.2007.12.005
DO - 10.1016/j.bbagrm.2007.12.005
M3 - Article
C2 - 18179780
AN - SCOPUS:40749100211
SN - 1874-9399
VL - 1779
SP - 164
EP - 174
JO - Biochimica et Biophysica Acta - Gene Regulatory Mechanisms
JF - Biochimica et Biophysica Acta - Gene Regulatory Mechanisms
IS - 3
ER -