The role of hormones in wound-stress response in Arabidopsis thaliana

hormones;wound stress;Arabidopsis

David, Lisa Illene ; Dr. Eric Davies, Committee Chair,Dr. Jose Alonso, Committee Member,Dr. Rebecca Boston, Committee Member,Dr. George Allen, Committee Member,David, Lisa Illene ; Dr. Eric Davies ; Committee Chair ; Dr. Jose Alonso ; Committee Member ; Dr. Rebecca Boston ; Committee Member ; Dr. George Allen ; Committee Member

University:North Carolina State University

关键词: hormones;    wound stress;    Arabidopsis;   

Others  :  https://repository.lib.ncsu.edu/bitstream/handle/1840.16/2174/etd.pdf?sequence=1&isAllowed=y

美国|英语

来源: null

【 摘 要 】

Wounding stress is a continuous threat to the survival of all organisms, and, in crop plants it leads to a dramatic reduction in crop yield. The signaling pathways that allow plants to respond to wounding stress are known to be complex. Many plant hormones such as jasmonic acid (JA), salicylic acid (SA), and ethylene have been identified as critical factors for the induction of wound-responsive genes in a number of plant species. However, the specific roles of each hormone in vivo, and how different hormones interact in the wound-stress response are largely unknown. Elucidation of the specific interactions of these plant hormones in response to wound stress is a major focus of wound research. The major goal of this research is to utilize Arabidopsis JA, SA, and ethylene biosynthetic and signaling mutants to analyze the role of each hormone separately and together in wound-responsive gene induction. Arabidopsis wild type, ein2, npr1, jar1, npr1/ein2, and npr1/jar1 plants were wounded and sampled at different times, after which RNA was extracted, subjected to electophoresis, transferred to filters and probed for several putative wound-regulated transcripts, which included PDF1.2, PR1, WAK1, and, LOX2. The constitutive levels of transcript expression as well as patterns of accumulation of these transcripts in response to the wounding stimulus varied in the different mutants.