Genome-wide analysis of gene expression profiling revealed that COP9 signalosome is essential for correct expression of Fe homeostasis genes in Arabidopsis

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dc.authorideroglu, seckin/0000-0002-9494-7080
dc.contributor.authorEroglu, Seckin
dc.contributor.authorAksoy, Emre
dc.date.accessioned2024-11-07T13:31:23Z
dc.date.available2024-11-07T13:31:23Z
dc.date.issued2017
dc.departmentNiğde Ömer Halisdemir Üniversitesi
dc.description.abstractIn plant cells, either excess or insufficient iron (Fe) concentration triggers stress responses, therefore it is strictly controlled. Proteasome-mediated degradation through ubiquitination of Fe homeostasis proteins has just become the focus of research in recent years. Deactivating ubiquitin ligases, COP9 signalosome has a central importance in the translational control of various stress responses. The aim of the study was to investigate COP9 signalosome in Fe deficiency response of Strategy I plants. In silico analysis of a set of Fe-deficiency-responsive genes was conducted against the transcriptome of Arabidopsis csn mutant lines using Genevestigator software. Induced and suppressed genes were clustered in a hierarchical way and gene ontology enrichment categories were identified. In wild-type Arabidopsis, CSN genes did not respond to iron deficiency. In csn mutant lines, under Fe-sufficient conditions, hundreds of Fe-deficiency-responsive genes were misregulated. Among the ones previously characterized for their physiological roles under Fe deficiency IRT1, NAS4, BTS, NRAMP1 were down-regulated while AHA2, MTP8, FRD3 were up-regulated. Unexpectedly, from those which were regulated in opposite ways, some had been repeatedly shown to be tightly co-regulated by the same transcription factor, FIT. Two proteins from DELLA family, which were reported to interact with FIT to repress its downstream, were found to be strikingly repressed in csn mutants. Overall, the study underlined that the absence of a functional CSN greatly impacted the regulation of Fe homeostasis-related genes, in a manner which cannot be explained simply by the induction of the master transcription factor, FIT. Correct expression of Fe deficiency-responsive genes requires an intact COP9 signalosome in Arabidopsis.
dc.description.sponsorshipScientific and Technological Council of Turkey [116C059]
dc.description.sponsorshipSeckin Eroglu thanks Scientific and Technological Council of Turkey (Ankara, Turkey) for the fellowship through BIDEB-2232 program (Project no: 116C059).
dc.identifier.doi10.1007/s10534-017-0036-8
dc.identifier.endpage698
dc.identifier.issn0966-0844
dc.identifier.issn1572-8773
dc.identifier.issue5
dc.identifier.pmid28744713
dc.identifier.scopus2-s2.0-85025814493
dc.identifier.scopusqualityQ1
dc.identifier.startpage685
dc.identifier.urihttps://doi.org/10.1007/s10534-017-0036-8
dc.identifier.urihttps://hdl.handle.net/11480/14823
dc.identifier.volume30
dc.identifier.wosWOS:000412955300005
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofBiometals
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_20241106
dc.subjectFIT
dc.subjectIron deficiency
dc.subjectMicroarray
dc.subjectDELLA
dc.subjectCOP9
dc.titleGenome-wide analysis of gene expression profiling revealed that COP9 signalosome is essential for correct expression of Fe homeostasis genes in Arabidopsis
dc.typeArticle

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