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Dissecting the role of pathogenesis related-10 (PR-10) proteins in abiotic stress tolerance of plants Open Access


Other title
pathogenesis related-10
abiotic stress
AP2 transcription factor
Type of item
Degree grantor
University of Alberta
Author or creator
Krishnaswamy, Sowmya
Supervisor and department
Dr. Nat Kav (Agricultural, Food and Nutritional Science, University of Alberta)
Examining committee member and department
Dr. Leluo Guan (Agricultural, Food and Nutritional Science, University of Alberta)
Dr. Wayne Snedden (Department of Biology, Queen’s University)
Dr. Stephen Strelkov (Agricultural, Food and Nutritional Science, University of Alberta)
Dr. Michael Deyholos (Biological Sciences, University of Alberta)
Department of Agricultural, Food and Nutritional Science

Date accepted
Graduation date
Doctor of Philosophy
Degree level
Abiotic stress is one of the major factors that affect food production worldwide and, therefore understanding stress responsive proteins and engineering plants for abiotic stress tolerance is very important. In the present study, the biological role of pea pathogenesis-related 10.4 (PR-10.4; also known as abscisic acid responsive 17; ABR17) in abiotic stress tolerance has been investigated. Our investigation on ribonuclease (RNase) activity of ABR17 suggested that highly conserved histidine-69 and glutamic acid-148 are important for RNase activity. In order to further investigate the biological role(s) of ABR17, transcriptional profiling of pea ABR17-mediated gene expression changes in ABR17-transgenic Arabidopsis thaliana plants was carried out using microarrays. Our results indicated that pea ABR17 modulates many plant growth/development genes most of which are cytokinin (CK) responsive. These results agree very well with previously reported enhanced endogenous CKs in these transgenic plants. However, no significant changes in transcript abundance of CK biosynthetic genes were observed between transgenic and wild-type plants, suggesting an alternate source of CK in ABR17-transgenic plants. It is speculated that ABR17 may act as either a CK reservoir (through its reported CK binding property) or may be responsible for isopentenylated-tRNA degradation (through its demonstrated RNase activity) thereby increasing endogenous CK pools. Furthermore, microarray analysis of salinity stressed ABR17-Arabidopsis indicated that ABR17 modulates many stress responsive genes that included four putative AP2 family genes (RAP2.6-At1g43160, RAP2.6L-At5g13330, DREB26-At1g21910 and DREB19-At2g38340). Functional characterization of these genes suggested that they are transcription factors and they play very important roles in abiotic stress response in addition to growth and development. Moreover, overexpression of RAP2.6L and DREB19 genes enhanced salinity and drought tolerance in Arabidopsis. Taken together, our results suggest that pea ABR17 proteins are important in abiotic stress responses as they may act as source of enhanced CKs and they may also modulate expression of stress responsive genes to enhance stress tolerance in plants. However, additional research aimed at deciphering the links between ABR17 and CK biosynthesis as well as the mechanism of ABR17-mediated gene expression changes should be conducted in order to get more insights into the biological roles of PR10 proteins in planta.
License granted by Sowmya Krishnaswamy ( on 2011-01-22 (GMT): Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of the above terms. The author reserves all other publication and other rights in association with the copyright in the thesis, and except as herein provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.
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