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Autor(en) / Beteiligte
Titel
KNAT7 positively regulates xylan biosynthesis by directly activating IRX9 expression in Arabidopsis
Ist Teil von
  • Journal of integrative plant biology, 2018-06, Vol.60 (6), p.514-528
Ort / Verlag
China (Republic : 1949- ): Wiley Subscription Services, Inc
Erscheinungsjahr
2018
Quelle
Alma/SFX Local Collection
Beschreibungen/Notizen
  • Xylan is the major plant hemicellulosic polysaccharide in the secondary cell wall. The transcription factor KNOTTED‐LIKE HOMEOBOX OF ARABIDOPSIS THALIANA 7 (KNAT7) regulates secondary cell wall biosynthesis, but its exact role in regulating xylan biosynthesis remains unclear. Using transactivation analyses, we demonstrate that KNAT7 activates the promoters of the xylan biosynthetic genes, IRREGULAR XYLEM 9 (IRX9), IRX10, IRREGULAR XYLEM 14‐LIKE (IRX14L), and FRAGILE FIBER 8 (FRA8). The knat7 T‐DNA insertion mutants have thinner vessel element walls and xylary fibers, and thicker interfascicular fiber walls in inflorescence stems, relative to wild‐type (WT). KNAT7 overexpression plants exhibited opposite effects. Glycosyl linkage and sugar composition analyses revealed lower xylan levels in knat7 inflorescence stems, relative to WT; a finding supported by labeling of inflorescence walls with xylan‐specific antibodies. The knat7 loss‐of‐function mutants had lower transcript levels of the xylan biosynthetic genes IRX9, IRX10, and FRA8, whereas KNAT7 overexpression plants had higher mRNA levels for IRX9, IRX10, IRX14L, and FRA8. Electrophoretic mobility shift assays indicated that KNAT7 binds to the IRX9 promoter. These results support the hypothesis that KNAT7 positively regulates xylan biosynthesis. KNAT7, as a transcription factor repressor, has been shown to negatively regulate secondary cell wall biosynthesis. In this study, we demonstrate that KNAT7 positively regulates xylan biosynthesis, which is one of the main components of secondary cell wall, by activating xylan biosynthesis genes IRX9, IRX10, IRX14L and FRA8.
Sprache
Englisch
Identifikatoren
ISSN: 1672-9072
eISSN: 1744-7909
DOI: 10.1111/jipb.12638
Titel-ID: cdi_wanfang_journals_zwxb201806007

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