دانلود رایگان ترجمه مقاله تنظیم الگوی گلدهی توسط ژن های زمان گلدهی (نشریه CellPress 2009)

تنظیم الگوی گلدهی توسط ژن های زمان گلدهی

Regulation of Floral Patterning by Flowering Time Genes

Abstract

Floral patterning in Arabidopsis requires activation of floral homeotic genes by the floral meristem identity gene, LEAFY (LFY). Here we show that precise activation of expression of class B and C homeotic genes in floral meristems is regulated by three flowering time genes, SHORT VEGETATIVE PHASE (SVP), SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 (SOC1), and AGAMOUS-LIKE 24 (AGL24), through direct control of a LFY coregulator, SEPALLATA3 (SEP3). Orchestrated repression of SEP3 by SVP, AGL24, and SOC1 is mediated by recruiting two interacting chromatin regulators, TERMINAL FLOWER 2/ LIKE HETEROCHROMATIN PROTEIN 1 and SAP18, a member of SIN3 histone deacetylase complex. Our finding of coordinated regulation of SEP3 by flowering time genes reveals a hitherto unknown genetic pathway that prevents premature differentiation of floral meristems and determines the appropriate timing of floral organ patterning.

۱ Introduction

Although flowers generated from different plant species are extensively diversified, the underlying genetic and molecular mechanisms that regulate flower development are highly conserved. InArabidopsis, our understanding of the mechanisms controlling flower development are encapsulated in the ‘‘ABC’’ model, which describes how each whorl of floral organs is determined by a combinatorial action of the A, B, and C class floral homeotic genes (Bowman et al., 1991; Coen and Meyerowitz, 1991). Further discovery of the SEPALLATA (SEP) genes has led to a revised ‘‘ABCE’’ model, in which the E class SEP genes function redundantly with other homeotic genes in specifying floral organs (Ditta et al., 2004; Goto et al., 2001; Pelaz et al., 2000; Theissen and Saedler, 2001).

A key regulator of early floral patterning is the floral meristem identity gene, LEAFY (LFY), which is expressed throughout young floral meristems and activates various floral homeotic genes in combination with other regulators (Parcy et al., 1998; Weigel et al., 1992). LFY directly activates APETALA1 (AP1), which plays dual roles in specifying the floral meristem and acting as a class A gene to determine the identity of perianth organs (Mandel et al., 1992; Wagner et al., 1999). Activation of a class B gene, APETALA3 (AP3), which determines petals and stamens, requires the concerted action of LFY, AP1, and UNUSUAL FLORAL ORGANS, an F box gene (Ng and Yanofsky, 2001; Parcy et al., 1998). LFY also cooperates with a homeobox gene, WUSCHEL (WUS), to activate the class C gene, AGAMOUS (AG), which specifies the identity of stamens and carpels (Lenhard et al., 2001; Lohmann et al., 2001). These observations have demonstrated an indispensable role of LFY in mediating early floral patterning, which leads to the spatially restricted expression of floral homeotic genes described in the ABC model.

Although the expression of class B and C genes is reduced in lfy-6 null mutants, their expression is not abolished (Weigel and Meyerowitz, 1993), indicating that some other factors may also contribute to activation of floral homeotic genes. In this study, we report that a genetic pathway mediated by three flowering time genes, SHORT VEGETATIVE PHASE (SVP), SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 (SOC1), and AGAMOUSLIKE 24 (AGL24), is required for the regulation of early floral patterning in Arabidopsis. These three genes encode closely related MADS box transcription factors involved in the control of flowering time (Hartmann et al., 2000; Lee et al., 2000; Michaels et al., 2003; Yu et al., 2002). In the emerging floral meristems, the expression of these genes is normally downregulated by AP1 to prevent the reversion of floral meristems into various shoot structures (Liu et al., 2007; Yu et al., 2004). Their single and double mutants produce normal flowers under standard growth temperature except for svp-41 agl24-2, in which several flowers at basal positions of the inflorescence show mild floral defects (Gregis et al., 2006). The defects are enhanced by growing at a higher temperature (e.g., 30C) or in the background of ap1 mutants, indicating the involvement of AP1 and these flowering time genes in flower development.

By investigating dramatic floral defects in the triple mutant soc1-2 agl24-1 svp-41, we have found that these three flowering time genes control floral patterning by directly preventing the ectopic expression of SEP3, a member of the class E genes, which acts with LFY to activate class B and C gene expression in stage 3 floral meristems. To maintain SEP3 chromatin in a silenced state, SVP interacts with TERMINAL FLOWER 2/LIKE HETEROCHROMATIN PROTEIN 1 (TFL2/LHP1) to modulate trimethylation of histone H3 lysine 27 (H3K27me3), while SOC1 and AGL24 interact with SAP18, a member of Sin3/histone deacetylase (HDAC) complex, to modulate histone H3 acetylation. Our results suggest that orchestrated repression of SEP3 by flowering time genes prevents premature differentiation of floral meristems and determines the timing of floral organ patterning.