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The Class II KNOX genes KNAT3 and KNAT7 work cooperatively to influence deposition of secondary cell walls that provide mechanical support to Arabidopsis stems
Author(s) -
Wang Shumin,
Yamaguchi Masatoshi,
Grienenberger Etienne,
Martone Patrick T.,
Samuels A. Lacey,
Mansfield Shawn D.
Publication year - 2020
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.14541
Subject(s) - xylem , arabidopsis , secondary cell wall , mutant , microbiology and biotechnology , transcription factor , cell wall , phenotype , homeobox , biology , gene , botany , genetics
Summary The transcription factor KNOTTED ARABIDOPSIS THALIANA7 ( KNAT7 ) is a Class II KNOTTED1‐like homeobox ( KNOX2 ) gene that, in interfascicular fibres, acts as a negative regulator of secondary cell wall biosynthesis. In addition, knat7 loss‐of‐function mutants display an irregular xylem ( irx ) phenotype, suggesting a potential positive regulatory role in xylem vessel secondary cell wall deposition. Although our understanding of the role of KNAT7 is evolving, the function(s) of the closely related KNOX2 genes, KNAT3 , KNAT4 , and KNAT5 , in secondary wall formation still remain unclear. We found that all four Arabidopsis KNOX2 genes were expressed in the inflorescence stems. However, only the knat3 knat7 double mutants showed a phenotype, displaying an enhanced irx phenotypes relative to the single mutants, as well as decreased interfascicular fibre cell wall thickness. Moreover, knat3 knat7 double mutants had reduced stem tensile and flexural strength compared with wild‐type and single mutants. In contrast, KNAT3 overexpression resulted in thicker interfascicular fibre secondary cell walls in inflorescence stems, suggesting a potential positive regulation in interfascicular fibre secondary wall development. This work identifies KNAT3 as a potential transcriptional activator working together with KNAT7 to promote secondary cell wall biosynthesis in xylem vessels, while concurrently acting antagonistically with KNAT7 to influence secondary wall formation in interfascicular fibres.