Premium
Brassinosteroids regulate outer ovule integument growth in part via the control of INNER NO OUTER by BRASSINOZOLE‐RESISTANT family transcription factors
Author(s) -
Jia Dandan,
Chen LianGe,
Yin Guimin,
Yang Xiaorui,
Gao Zhihua,
Guo Yi,
Sun Yu,
Tang Wenqiang
Publication year - 2020
Publication title -
journal of integrative plant biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.734
H-Index - 83
eISSN - 1744-7909
pISSN - 1672-9072
DOI - 10.1111/jipb.12915
Subject(s) - integument , ovule , mutant , biology , microbiology and biotechnology , transcription factor , arabidopsis , arabidopsis thaliana , gene , gene expression , transcription (linguistics) , genetics , embryo , botany , linguistics , philosophy
Brassinosteroids (BRs) play important roles in regulating plant reproductive processes. BR signaling or BR biosynthesis null mutants do not produce seeds under natural conditions, but the molecular mechanism underlying this infertility is poorly understood. In this study, we report that outer integument growth and embryo sac development were impaired in the ovules of the Arabidopsis thaliana BR receptor null mutant bri1‐116 . Gene expression and RNA‐seq analyses showed that the expression of INNER NO OUTER ( INO ), an essential regulator of outer integument growth, was significantly reduced in the bri1‐116 mutant. Increased INO expression due to overexpression or increased transcriptional activity of BRASSINAZOLE‐RESISTANT 1 (BZR1) in the mutant alleviated the outer integument growth defect in bri1‐116 ovules, suggesting that BRs regulate outer integument growth partially via BZR1‐mediated transcriptional regulation of INO . Meanwhile, INO expression in bzr‐h , a null mutant for all BZR1 family genes, was barely detectable; and the outer integument of bzr‐h ovules had much more severe growth defects than those of the bri1‐116 mutant. Together, our findings establish a new role for BRs in regulating ovule development and suggest that BZR1 family transcription factors might regulate outer integument growth through both BRI1‐dependent and BRI1‐independent pathways.