Open AccessSuppression of class I compensated cell enlargement by xs2 mutation is mediated by salicylic acid signaling
Author(s) -
Ushio Fujikura,
Kazune Ezaki,
Gorou Horiguchi,
Mitsunori Seo,
Yuka Kanno,
Yûji Kamiya,
Michael Lenhard,
Hirokazu Tsukaya
Publication year - 2020
Publication title -
plos genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.587
H-Index - 233
eISSN - 1553-7404
pISSN - 1553-7390
DOI - 10.1371/journal.pgen.1008873
Subject(s) - salicylic acid , mutant , biology , arabidopsis , microbiology and biotechnology , cell growth , mutation , cell , positional cloning , genetic screen , cell division , signal transduction , genetics , gene
The regulation of leaf size has been studied for decades. Enhancement of post-mitotic cell expansion triggered by impaired cell proliferation in Arabidopsis is an important process for leaf size regulation, and is known as compensation. This suggests a key interaction between cell proliferation and cell expansion during leaf development. Several studies have highlighted the impact of this integration mechanism on leaf size determination; however, the molecular basis of compensation remains largely unknown. Previously, we identified extra-small sisters ( xs ) mutants which can suppress compensated cell enlargement (CCE) via a specific defect in cell expansion within the compensation-exhibiting mutant, angustifolia3 ( an3 ). Here we revealed that one of the xs mutants, namely xs2 , can suppress CCE not only in an3 but also in other compensation-exhibiting mutants erecta ( er ) and fugu2 . Molecular cloning of XS2 identified a deleterious mutation in CATION CALCIUM EXCHANGER 4 ( CCX4 ). Phytohormone measurement and expression analysis revealed that xs2 shows hyper activation of the salicylic acid (SA) response pathway, where activation of SA response can suppress CCE in compensation mutants. All together, these results highlight the regulatory connection which coordinates compensation and SA response.