Promoter analysis of a subfamily of calmodulin-like gene in Arabidopsis
Thesis (Master, Biology) -- Queen's University, 2009-09-10 13:10:31.576 === Ca2+ ions participate as second messengers in many stress-response and developmental pathways. Among eukaryotes, plants possess a remarkable diversity of Ca2+ binding proteins (Ca2+ sensors) such as calmodulin (CaM) and...
Main Author: | |
---|---|
Other Authors: | |
Format: | Others |
Language: | en en |
Published: |
2009
|
Subjects: | |
Online Access: | http://hdl.handle.net/1974/5205 |
Summary: | Thesis (Master, Biology) -- Queen's University, 2009-09-10 13:10:31.576 === Ca2+ ions participate as second messengers in many stress-response and developmental pathways. Among eukaryotes, plants possess a remarkable diversity of Ca2+ binding proteins (Ca2+ sensors) such as calmodulin (CaM) and CaM-related proteins (CMLs) that regulate downstream targets and coordinate signal transduction events in response to stimuli. Previous studies have shown that a small subfamily of CMLs (CML37, CML38, CML39) in Arabidopsis show differential tissue expression as well as a dramatic induction of expression in response to environmental stress. For example, CML37 and CML38 respond very strongly to wounding, while CML39 is induced significantly by jasmonate. In order to understand the underlying regulatory mechanisms of the genes, promoter analysis experiments using the 5 upstream regions of these CMLs driving -glucuronidase (GUS) reporter expression were conducted. This empirical approach is a critical complement to algorithm-based prediction methods. It was found that the gateway vector pMDC163 was unsuitable for 5 deletion analyses. Three regions within the CML37 promoter were identified as having wound-responsiveness. Several known wound-responsive cis-elements were identified in these regions. A putative cis-element that is overrepresented in genes coexpressed with CML37 was also identified. Together, these data should lay the groundwork to identify the transcriptional regulators that direct stress-responsive CML gene expression. === Master |
---|