Abstract
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.
Highlights
Understanding how organ size is regulated in plants has remained as a fundamental question in the field of plant science over the last few decades
Recent studies highlighted the existence of integrated mechanism which coordinates cell proliferation and cell expansion during leaf development
Kinematic analysis of several compensation-exhibiting mutants revealed that abnormal cell enlargement, termed “compensated cell enlargement (CCE)” can be classified into three classes based on their way of development [13, 20]
Summary
Understanding how organ size is regulated in plants has remained as a fundamental question in the field of plant science over the last few decades. Several studies have highlighted the phenomenon of “compensation”, which refers to a decrease in cell number accompanied with a significant increase in cell size, caused by a mutation or ectopic expression of a particular transgene. These findings suggest that the two spatially separated events, cell proliferation and cell expansion are highly coordinated during leaf development [7, 10,11,12,13,14,15,16,17,18,19]. Another difference is that compensation is mediated in a cell-autonomous and a non-cell-autonomous manner in the KRP2ox and an, respectively, as Kawade et al have demonstrated [21]
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