SummaryIn all eukaryotes chromatin physically restricts the accessibility of the genome to regulatory proteins such as transcription factors. Plant model systems have been instrumental in demonstrating that this restriction is dynamic and changes during development and in response to exogenous cues. Among the multiple epigenetic mechanisms that alter chromatin to regulate gene expression, histone modifications play a major role. Recent studies in Arabidopsis have provided the first genome-wide histone modification maps, revealed important biological roles for histone modifications, and advanced our understanding of stimulus-dependent changes in histone modifications.
Chromatin remodeling is emerging as a central mechanism for patterning and differentiation in multicellular eukaryotes. SWI/SNF chromatin remodeling ATPases are conserved in the animal and plant kingdom and regulate transcriptional programs in response to endogenous and exogenous cues. In contrast with their metazoan orthologs, null mutants in two Arabidopsis thaliana SWI/SNF ATPases, BRAHMA (BRM) and SPLAYED (SYD), are viable, facilitating investigation of their role in the organism. Previous analyses revealed that syd and brm null mutants exhibit both similar and distinct developmental defects, yet the functional relationship between the two closely related ATPases is not understood. Another central question is whether these proteins act as general or specific transcriptional regulators. Using global expression studies, double mutant analysis, and protein interaction assays, we find overlapping functions for the two SWI/SNF ATPases. This partial diversification may have allowed expansion of the SWI/SNF ATPase regulatory repertoire, while preserving essential ancestral functions. Moreover, only a small fraction of all genes depends on SYD or BRM for expression, indicating that these SWI/SNF ATPases exhibit remarkable regulatory specificity. Our studies provide a conceptual framework for understanding the role of SWI/SNF chromatin remodeling in regulation of Arabidopsis development.
The CUP-SHAPED COTYLEDON (CUC) genes CUC1, CUC2 and CUC3 act redundantly to control cotyledon separation in Arabidopsis. In order to identify novel regulators of this process, we have performed a phenotypical enhancer screen using a null allele of cuc2, cuc2-1. We identified three nonsense alleles of AtBRM, an Arabidopsis SWI/SNF chromatin remodeling ATPase, that result in strong cotyledon fusion in cuc2-1. atbrm also enhances cotyledon fusion in loss-of-function cuc1 and cuc3 mutants, suggesting a general requirement for this ATPase in cotyledon separation. By contrast, a null allele of SPLAYED (SYD), the closest homolog of AtBRM in Arabidopsis, enhances only the loss-of-function cuc1 mutant. By investigating the activities of the CUC promoters in the cotyledon boundary during embryogenesis in sensitized backgrounds, we demonstrate that AtBRM upregulates the transcription of all three CUC genes, whereas SYD upregulates the expression of CUC2. Our results uncover a specific role for both chromatin remodeling ATPases in the formation and/or maintenance of boundary cells during embryogenesis. Development 133, 3223-3230 (2006) DEVELOPMENT 3224 and the complex composition of the SWI/SNF remodelers is becoming better understood, understanding their role in the organism has been hampered by the fact that mutations in most SWI/SNF ATPases are embryo lethal (Bultman et al., 2000; Bultman et al., 2005;Indra et al., 2005;Reyes et al., 1998;Sawa et al., 2000;Tamkun et al., 1992). We show here that the two SWI/SNF ATPases AtBRM and SYD are specifically and differentially required for cotyledon separation in Arabidopsis via the regulation of expression of a small gene family. KEY WORDS: Arabidopsis, Embryo, Boundary formation, CUP-SHAPED COTYLEDON, Chromatin remodeling ATPase MATERIALS AND METHODS Plant lines and growth conditionscuc2-1, stm-1, stm-2, cuc1-1 and syd-2 mutants have been described (Aida et al., 1997; Barton and Poethig, 1993; Clark et al., 1996;Takada et al., 2001;Wagner and Meyerowitz, 2002). stm-2 syd-2 was described in a previous study (Kwon et al., 2005). cuc3-101, isolated as an enhancer mutant of cuc2-1, carries a point mutation at the junction of the first exon and intron (AG:GT to AG:AT) and represents a strong allele (K.i.-H., M.A. and M.T., unpublished). Double-mutant plants made in this study were genotyped for cuc1 -1, cuc3-101, syd-2, stm-2, atbrm-1, atbrm-2 and atbrm-3 using dCAPS. Homozygous cuc2-1 was genotyped by amplifying a genomic DNA region flanking the transposon insertion site (Aida et al., 1997). Segregating populations of syd-2 and atbrm-1 were individually maintained in Ler, cuc1-1, cuc2-1 and cuc3-101 homozygous backgrounds. stm-2 atbrm-1 was maintained as double heterozygotes. Seeds were sown on fertilized soil mix (Promix BX; Premier Horticulture, Quakertown, PA), stratified in the dark at 4°C for 7 days, and then grown at 22°C in long day (16 hours light) conditions at 120 mol/m 2 sec of cool white light. Plants were photographed using an Olympus SZX12 dissecting microscope e...
implicate SEU in auxin-regulated growth and development. seu has a pleiotropic phenotype that includes reductions in several classic auxin responses such as apical dominance, lateral root initiation, sensitivity to exogenous auxin and activation of the DR5 auxin response reporter. seu displays a synergistic interaction with the auxin response mutant pinoid, producing flowers with few outer whorl organs. Collectively, these data suggest that SEU is a novel factor affecting auxin response. A model is proposed in which SEU functions jointly with ETT in auxin response to promote floral organ patterning and growth.
Summary SWI2/SNF2 chromatin remodeling ATPases play important roles in plant and metazoan development. While metazoans generally encode one or two SWI2/SNF2 ATPase genes, Arabidopsis encodes four such chromatin regulators: the well-studied BRAHMA and SPLAYED ATPases as well as two closely related non-canonical SWI2/SNF2 ATPases, CHR12 and CHR23. No developmental role has as yet been described for CHR12 and CHR23. Here we show that while strong single chr12 or chr23 mutants are morphologically indistinguishable from the wild type, chr12 chr23 double mutants cause embryonic lethality. The double mutant embryos fail to initiate root and shoot meristems and display few and aberrant cell division. Weak double mutant embryos give rise to viable seedlings with dramatic defects in the maintenance of both the shoot and the root stem cell populations. Paradoxically, the stem cell defects are correlated with increased expression of the stem cell markers WUSCHEL and WOX5. During subsequent development, the meristem defects are partially overcome to allow for the formation of very small, bushy adult plants. Based on the observed morphological defects we named the two chromatin remodelers MINUSCULE 1 and 2. Possible links between minu1 minu2 defects and defects in hormone signaling and replication-coupled chromatin assembly are discussed.
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