Poster: Regulation of gene expression

Abs # 742: An Arabidopsis homeodomain transcription factor gene, HOS9 mediates cold tolerance through a novel pathway

Presenter:	Zhu, Jianhua , jhzhu@purdue.edu
Authors	Zhu, Jianhua  (A)   Shi, Huazhong  (A)   Lee, Byeong-ha  (B)   Damsz, Barbara  (A)   Cheng, Shie  (A)   Stirm, Vicki  (A)   Zhu, Jian-Kang  (B)   Hasegawa, Paul M (A)   Bressan, Ray A (A)
Affiliations:	(A): Purdue University, Department of Horticulture (B): University of Arizona, Department of Plant Sciences

To investigate essential components mediating stress signaling in plants, we initiated a large scale stress response screen using Arabidopsis plants carrying the firefly luciferase reporter gene under the control of the stress-responsive RD29A promoter. Here we report the identification and characterization of a mutant, hos9-1 (for high expression of osmotically responsive genes) in which the reporter construct was hyperactivated by low temperature, but not by abscisic acid (ABA) or salinity stress. The mutants grow more slowly, and flower later, than do wild type plants; and are more sensitive to freezing, both before and after acclimation, than the wild type plants. The HOS9 gene encodes a putative homeodomain transcription factor that is localized to the nucleus. HOS9 is constitutively expressed and not further induced by cold stress. Cold treatment increased the level of transcripts of the endogenous RD29A, and some other stress-responsive genes, to a higher level in hos9-1 than in wild type plants. However, the CBF (CRT/DRE binding factor) transcription factor genes that mediate a part of cold acclimation in Arabidopsis did not have their response to cold altered by the hos9-1 mutation. Correspondingly, micro array analysis showed that none of the genes affected by the hos9-1 mutation are controlled by the CBF family. Together, these results suggest that HOS9 is important for plant growth and development, and for a part of freezing tolerance, by affecting the activity of genes independent of the CBF pathway.