ERECTA Family Genes Regulate Auxin Transport in the Shoot Apical Meristem and Forming Leaf Primordia

Abstract

Leaves are produced postembryonically at the flanks of the shoot apical meristem. Their initiation is induced by a positive feedback loop between auxin and its transporter PIN-FORMED1 (PIN1). The expression and polarity of PIN1 in the shoot apical meristem is thought to be regulated primarily by auxin concentration and flow. The formation of an auxin maximum in the L1 layer of the meristem is the first sign of leaf initiation and is promptly followed by auxin flow into the inner tissues, formation of the midvein, and appearance of the primordium bulge. The ERECTA family genes (ERfs) encode leucine-rich repeat receptor-like kinases, and in Arabidopsis (Arabidopsis thaliana), this gene family consists of ERECTA (ER), ERECTA-LIKE1 (ERL1), and ERL2. Here, we show that ERfs regulate auxin transport during leaf initiation. The shoot apical meristem of the er erl1 erl2 triple mutant produces leaf primordia at a significantly reduced rate and with altered phyllotaxy. This phenotype is likely due to deficiencies in auxin transport in the shoot apex, as judged by altered expression of PIN1, the auxin reporter DR5rev::GFP, and the auxininducible genes MONOPTEROS, INDOLE-3-ACETIC ACID INDUCIBLE1 (IAA1), and IAA19. In er erl1 erl2, auxin presumably accumulates in the L1 layer of the meristem, unable to flow into the vasculature of a hypocotyl. Our data demonstrate that ERfs are essential for PIN1 expression in the forming midvein of future leaf primordia and in the vasculature of emerging leaves.

The Yin-Yang of Hormones: Cytokinin and Auxin Interactions in Plant Development

“…Similarly, a mutation in rice that reduces cytokinin sensitivity results in a larger shoot meristem and altered leaf phyllotaxy (Itoh et al, 2012). In Arabidopsis, the ERECTA family of genes, which are implicated in buffering the SAM against changes in cytokinin levels (Uchida et al, 2013), also play a role in organ initiation and phyllotaxy through effects on auxin flux, apparently due to a role in establishing the appropriate PIN expression pattern (Chen et al, 2013). These effects of ERECTA correlate with changes in the SAM size, but also suggest that the ERECTA family may play a significant, but largely unexplored role, in mediating the crosstalk between auxin and cytokinin.…”

CLAVATA-WUSCHEL signaling in the shoot meristem

“…ER is expressed in the SAM, and although er mutants do not exhibit any obvious meristem phenotype, mutants of ER and its family members ERECTA-LIKE1 and ERECTA-LIKE2 enhance clv meristem phenotypes (Durbak and Tax, 2011;Torii et al, 1996;Yokoyama et al, 1998). These effects of mutations in ER family genes on meristem size are the result of enhanced WUS expression, possibly via an HD-ZIPIIIdependent but CLV-independent signaling pathway (Chen et al, 2013;Mandel et al, 2014). In a more recent study, using mutant combination analysis with 2D sectioning of meristems, it was hypothesized that CLV3 controls meristem expansion along the apical-basal axis, while the ER family members control lateral expansion in a perpendicular orientation (Mandel et al, 2016).…”

FASCIATED EAR4Encodes a bZIP Transcription Factor That Regulates Shoot Meristem Size in Maize

“…In addition, FEA4 and KN1 bound and positively modulated a CUC-like NAC TF (GRMZM2G430522), consistent with positive regulation of CUC genes by SHOOT MERISTEMLESS in Arabidopsis (Spinelli et al, 2011), an LRR kinase (GRMZM5G809695) with sequence similarity to ERECTA and implicated in specification of organs originating at the SAM (Torii et al, 1996;Mandel et al, 2014), and a NPH3 domain protein (GRMZM2G067053) similar to ENHANCER OF PINOID. The latter two have been implicated in regulation of auxin transport (Treml et al, 2005;Chen et al, 2013). While FEA4 and KN1 share largely overlapping expression patterns with both excluded from the P 0 (Jackson et al, 1994), KN1 is expressed in the central zone, whereas FEA4 is not.…”