Premium
PAG1 , a cotton brassinosteroid catabolism gene, modulates fiber elongation
Author(s) -
Yang Zuoren,
Zhang Chaojun,
Yang Xiaojie,
Liu Kun,
Wu Zhixia,
Zhang Xueyan,
Zheng Wu,
Xun Qingqing,
Liu Chuanliang,
Lu Lili,
Yang Zhaoen,
Qian Yuyuan,
Xu Zhenzhen,
Li Changfeng,
Li Jia,
Li Fuguang
Publication year - 2014
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.12824
Subject(s) - microbiology and biotechnology , biology , gene expression , biochemistry , gene
Summary Cotton ( G ossypium hirsutum ) is the major source of natural textile fibers. Brassinosteroids ( BR s) play crucial roles in regulating fiber development. The molecular mechanisms of BR s in regulating fiber elongation, however, are poorly understood. pagoda1 (pag1) was identified via an activation tagging genetic screen and characterized by genome walking and brassinolide ( BL ) supplementation. RNA ‐Seq analysis was employed to elucidate the mechanisms of PAG 1 in regulating fiber development. pag1 exhibited dwarfism and reduced fiber length due to significant inhibition of cell elongation and expansion. BL treatment rescued its growth and fiber elongation. PAG 1 encodes a homolog of Arabidopsis CYP 734A1 that inactivates BR s via C‐26 hydroxylation. RNA ‐Seq analyses showed that the constitutive expression of PAG 1 downregulated the expression of genes involved in very‐long‐chain fatty acids ( VLCFA ) biosynthesis, ethylene‐mediated signaling, response to cadmium, cell wall development, cytoskeleton organization and cell growth. Our results demonstrate that PAG 1 plays crucial roles in regulating fiber development via controlling the level of endogenous bioactive BR s, which may affect ethylene signaling cascade by mediating VLCFA . Therefore, BR may be a critical regulator of fiber elongation, a role which may in turn be linked to effects on VLCFA biosynthesis, ethylene and cadmium signaling, cell wall‐ and cytoskeleton‐related gene expression.