Non-cell-autonomously coordinated organ size regulation in leaf development

Abstract

SUMMARYThe way in which the number and size of cells in an organ are determined poses a central challenge in our understanding of organ size control. Compensation is an unresolved phenomenon, whereby a decrease in cell proliferation below some threshold level triggers enhanced postmitotic cell expansion in leaf primordia. It suggests an interaction between these cellular processes during organogenesis and provides clues relevant to an understanding of organ size regulation. Although much attention has been given to compensation, it remains unclear how the cellular processes are coordinated. Here, we used a loss-of-function mutation in the transcriptional coactivator gene ANGUSTIFOLIA3 (AN3), which causes typical compensation in Arabidopsis thaliana. We established Cre/lox systems to generate leaves chimeric for AN3 expression and investigated whether compensation occurs in a cell-autonomous or non-cell-autonomous manner. We found that an3-dependent compensation is a non-cellautonomous process, and that an3 cells seem to generate and transmit an intercellular signal that enhances postmitotic cell expansion. The range of signalling was restricted to within one-half of a leaf partitioned by the midrib. Additionally, we also demonstrated that overexpression of the cyclin-dependent kinase inhibitor gene KIP-RELATED PROTEIN2 resulted in cellautonomous compensation. Together, our results revealed two previously unknown pathways that coordinate cell proliferation and postmitotic cell expansion for organ size control in plants.

Genetic Dissection of Leaf Development in Brassica rapa Using a Genetical Genomics Approach

“…copQTL15 (LBs, Pmh, LW, and LI) colocalized with a cis-eQTL for BrKRP2_A03, another cis-eQTL for BrGTE6_A03, and five trans-eQTLs for BRASSICA RAPA CELL DIVISION CONTROL2_A01.2 (BrCDC2_A01.2), BrCDC2_A06.2, BRASSICA RAPA PHABULOSA_A04 (BrPHB_A04), BrCycD3;2_A07, and BrGA20OX3_A10 (Table IV). KRP2 and GTE6 play roles in organ size and leaf development in Arabidopsis (Chua et al, 2005;Kawade et al, 2010). The PHB transcription factor causes the transformation of abaxial to adaxial leaf fates (Bao et al, 2004).…”

“…Among of them, BrARGOS_A09 and BrARL_A03 influence cell size and are up-regulated by brassinosteroids (Hu et al, 2006;Feng et al, 2011), while another report describes that auxin acts via the ARGOS protein to regulate leaf size (Hay et al, 2004). BrKRP2_A03.2 was involved in the regulation of cell proliferation and postmitotic cell expansion to control organ size in Arabidopsis (Kawade et al, 2010). The other six traits in this subnetwork are associated with genes from four functional pathways, including five genes involved in LL, three genes involved with adaxial-abaxial polarity, one symmetry gene BRASSICA RAPA GENERAL TRAN-SCRIPTION FACTOR GROUP E6_A03 (BrGTE6_A03), and two "other" pathway genes (BrAE3_A02 and Table S6).…”

Stable establishment of cotyledon identity during embryogenesis in Arabidopsis by ANGUSTIFOLIA3 and HANABA TARANU

“…Compensation is an event that increases cell size in response to a reduction in leaf cell number due to a genetic defect (Tsukaya, 2002;Beemster et al, 2003;Tsukaya, 2008;. The an3-induced compensation is mediated non-cell autonomously (Horiguchi et al, 2005;Ferjani et al, 2007;Fujikura et al, 2007;Fujikura et al, 2009;Lee et al, 2009;Kawade et al, 2010). AN3 is also involved in leaf patterning.…”

Kinematic evidence that atmospheric nitrogen dioxide increases the rates of cell proliferation and enlargement to stimulate leaf expansion in Arabidopsis

“…This result agrees with the general idea that the size of an organ is determined by the number and size of its constituent cells. [8][9][10] The peak values of the RLER, RCDR and RCER were always greater in CNO 2 plants compared to corresponding values in -NO 2 plants (Fig. 1D, E and F, respectively) ), respectively.…”