Involvement of the Fas-associated Factor1 Ortholog, CaFAF1, in Regulating Programmed Cell Death in Plants
- Authors
- Kim, Young Jin; Park, Chang-Jin; Ham, Byung-Kook; Paek, Kyung-Hee
- Issue Date
- 4월-2009
- Publisher
- SPRINGER HEIDELBERG
- Keywords
- Capsicum annuum L.; Hypersensitive response; Pepper mild mottle virus (PMMoV); Programmed cell death (PCD); Virus-induced gene silencing
- Citation
- JOURNAL OF PLANT BIOLOGY, v.52, no.2, pp.125 - 134
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- JOURNAL OF PLANT BIOLOGY
- Volume
- 52
- Number
- 2
- Start Page
- 125
- End Page
- 134
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/120311
- DOI
- 10.1007/s12374-009-9012-3
- ISSN
- 1226-9239
- Abstract
- Programmed cell death (PCD) in plant cells is often accompanied by biochemical and morphological hallmarks similar to those of animal apoptosis. However, orthologs of several core components of such apoptosis have not been reported in plants. Here, we describe an ortholog of Fas-associated factor1 (FAF1), a member of the Fas-death-inducing signaling complex (Fas-DISC), found in pepper. We also examined FAF1 orthologs in other plant species. Transcripts of CaFAF1 specifically accumulated in pepper leaves infected with the avirulent pepper mild mottle virus (PMMoV) P-0 pathotype. This gene was also strongly expressed in aging leaves. To determine whether those orthologs are involved in PCD, we suppressed their expression through virus-induced gene silencing, and determined the effect on the hypersensitive response (HR), a typical PCD, in pepper, tomato, and tobacco. Constitutive expression of CaFAF1 in transgenic tobacco triggered spontaneous induction of cell death lesions and induced pathogenesis-related (PR) genes. This ability to cause cell death and suppress R gene-mediated HR in its knockdown condition suggests that some features of animal and plant cell death processes may be shared. We propose that plant FAF1 is a conserved cell death regulator in both kingdoms.
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Collections - College of Life Sciences and Biotechnology > Division of Life Sciences > 1. Journal Articles
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