Comparative microarray analysis of programmed cell death induced by proteasome malfunction and hypersensitive response in plants

Cited 16 time in scopus
Metadata Downloads

Full metadata record

DC FieldValueLanguage
dc.contributor.authorMoonil Kim-
dc.contributor.authorSanghyeob Lee-
dc.contributor.authorKyoungsook Park-
dc.contributor.authorEun-Ju Jeong-
dc.contributor.authorChoong-Min Ryu-
dc.contributor.authorDoil Choi-
dc.contributor.authorH S Pai-
dc.description.abstractProgrammed cell death (PCD) plays a pivotal role in the elimination of injured or unwanted cells during diverse physiological and developmental conditions in organisms. However in contrast to the animal system, signaling pathways and molecular mechanism of PCD are largely unknown in plants. We previously reported that silencing of NbPAF encoding the α6 subunit of 20S proteasome by virus-induced gene silencing activated programmed cell death in plants by inactivating proteasome function. In this study, we analyzed global gene expression profile of PCD induced by suppression of NbPAF expression, in comparison with that of hypersensitive response (HR)-induced PCD, using a cDNA microarray representing 4685 hot pepper genes. HR is a well-characterized PCD program in plants, which occurs in response to pathogen infection. The microarray analyses identified 247 genes whose gene expression was differentially modulated during PCD activated by NbPAF depletion or HR. Most of the genes that were up-regulated during the NbPAF-mediated PCD, including the ubiquitin/proteasome pathway-related genes, were down-regulated during HR cell death. In contrast, transcription of many defense-related genes, transcription factor genes, and photosynthesis-related genes remained unchanged or repressed during NbPAF-mediated PCD, while it was highly induced during HR cell death. Only a small number of genes including antioxidant-related genes and proteases were found to be up-regulated during induction of PCD by both proteasome inactivation and HR. Based on these results, these two PCD pathways appear to be differentially regulated, but some overlapping mechanism exists, which involves core regulators of plant PCD.-
dc.titleComparative microarray analysis of programmed cell death induced by proteasome malfunction and hypersensitive response in plants-
dc.title.alternativeComparative microarray analysis of programmed cell death induced by proteasome malfunction and hypersensitive response in plants-
dc.citation.titleBiochemical and Biophysical Research Communications-
dc.contributor.affiliatedAuthorMoonil Kim-
dc.contributor.affiliatedAuthorSanghyeob Lee-
dc.contributor.affiliatedAuthorKyoungsook Park-
dc.contributor.affiliatedAuthorEun-Ju Jeong-
dc.contributor.affiliatedAuthorChoong-Min Ryu-
dc.contributor.affiliatedAuthorDoil Choi-
dc.identifier.bibliographicCitationBiochemical and Biophysical Research Communications, vol. 342, no. 2, pp. 514-521-
dc.subject.keywordα6 Subunit of 20S proteasome-
dc.subject.keywordcDNA microarray-
dc.subject.keywordGene expression-
dc.subject.keywordHot pepper-
dc.subject.keywordHypersensitive response-
dc.subject.keywordVirus-induced gene silencing-
dc.subject.localα6 Subunit of 20S proteasome-
dc.subject.localcDNA micro-array-
dc.subject.localcDNA microarray-
dc.subject.localGene Expression-
dc.subject.localGene expression-
dc.subject.localgene expression-
dc.subject.localhot pepper-
dc.subject.localHot pepper-
dc.subject.localhypersensitive response-
dc.subject.localHypersensitive response-
dc.subject.localHypersensitive Response-
dc.subject.localVirus-induced gene silencing (VIGS)-
dc.subject.localvirus-induced gene silencing-
dc.subject.localVirus-induced gene silencing-
Appears in Collections:
Critical Diseases Diagnostics Convergence Research Center > 1. Journal Articles
Division of Research on National Challenges > Infectious Disease Research Center > 1. Journal Articles
Files in This Item:
  • There are no files associated with this item.

Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.