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The SBP transcription factor SPL10 regulates leaf curvature by promoting REVOLUTA transcription in plants

ABSTRACT: The SBP transcription factor SPL10 regulates leaf curvature by promoting REVOLUTA transcription in plants

PROVIDER: PRJNA1052585 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27205582_1.fastq.gz	Fastqsanger.gz
	SRR27205582_2.fastq.gz	Fastqsanger.gz
	SRR27205583_1.fastq.gz	Fastqsanger.gz
	SRR27205583_2.fastq.gz	Fastqsanger.gz
	SRR27205584_1.fastq.gz	Fastqsanger.gz

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The SBP transcription factor SPL10 regulates leaf curvature by promoting REVOLUTA transcription in plants

Project description:The developmental functions of SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) 10 have been extensively studied in Arabidopsis, but SPL10's role in regulating leaf curvature has not been well characterized. In this study, we observed an upward-curling leaf phenotype upon overexpression of a miR156/157-resistant version of SPL10 (rSPL10). DNA affinity purification sequencing (DAP-seq), RNA-seq, and transient transactivation assays revealed that SPL10 binds to the promoter of REVOLUTA (REV). Consistent with binding assays, overexpression of a miR165/166-resistant version of REV (rREV) in WT plants caused an upward-curling leaf phenotype. Conversely, overexpression of rSPL10 in a rev-6 mutant couldn't rescue the downward-curling leaf phenotype of rev-6. Notably, SPL10 physically interacts with REV, attenuating the upward-curling leaf phenotype of rREV mutants, suggesting a role as a molecular rheostat to prevent overamplification of REV transcripts. Furthermore, overexpression of the BrpREV-1 gene caused rosette leaves to change from flat to upward curving and accelerated heading in Chinese cabbage. Taken together, our findings identify the role of the SPL10-REV module in regulating leaf curvature in Arabidopsis and the crucial functions of BrpREV-1 in the heading of Chinese cabbage.

2024-06-20 | GSE250168 | GEO

CINCINNATA Controls Surface Curvature of Antirrhinum Leaf by Coordinated and Direct Activation of Cytokinin and Auxin Signaling

Project description:Mutations in the CINCINNATA gene in Antirrhinum and its orthologues in Arabidopsis cause negative surface curvature in leaves due to excess marginal growth. CIN-like genes code for TCP transcription factors and are expressed in a broad zone of a growing leaf somewhat distal to the proliferation zone. Although a few TCP targets are known, the role of CIN-like TCP genes in regulating leaf curvature has remained unclear. We have compared the global transcription profile of wild type and cincinnata mutant to identify its targets. By combining DNA-protein interaction, chromatin immunoprecipitation and RNA in situ hybridization, we show that CIN maintains surface flatness by regulating signaling or level of major plant hormones. CIN promotes cytokinin signaling directly and GA level indirectly, in accelerating maturity in leaf cells along the tip-to-base direction. In addition, CIN suppresses auxin signaling more at the margin than centre by establishing a margin-to-medial expression gradient of a homologue of the auxin suppressor IAA3. Our results uncover an underlying mechanism in a developing leaf that controls maturity of leaf and its surface curvature. Considering the conservation of CIN-like genes and their function in leaf morphogenesis in multiple plant species, it is likely that such mechanism is evolutionarily conserved.

2013-05-01 | GSE40621 | GEO

CINCINNATA Controls Surface Curvature of Antirrhinum Leaf by Coordinated and Direct Activation of Cytokinin and Auxin Signaling

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A direct link between Prss53, hair curvature, and skeletal dysplasia

Project description:PRSS53, a member of the membrane-anchored serine proteases, hydrolyzes peptide bonds and is highly expressed in the hair follicle IRS, medulla, precortex and some melanocytes1. Previous studies reported that Prss53 is a psoriasis susceptibility locus and is linked to systemic lupus erythematosus, suggesting its potential roles in skin function2. The Q30R SNP in Prss53 may influence hair shape and is involved in the human variation of head hair shape among different continental groups1. In addition, ENaC activity is regulated by the activity of a channel-activating protease of Prss8 (a homologous gene of Prss53), implying the Prss53 may have an indispensable role in ion channel activity3.The triggering of hair curvature is clearly related to symmetry or asymmetry axis formation in follicles and includes Wnt, TGFβ, BMP, Shh and FGFs, etc. In particular, the Wnt/Ca2+ and Wnt/planar cell polarity (PCP) pathways are additional novel mechanisms that affect hair shape4. Furthermore, disruptions in calcium metabolism may contribute to a wide variety of clinical symptoms, including osteoporosis, osteolysis, nephrocalcinosis and adynamie5.Here, we successfully generated Prss53-deficient rabbits. These rabbits exhibited curved hair, severe skeletal malformation and disrupted calcium metabolism. Altogether, these data suggest that Prss53 play an important role in calcium metabolism and provide the first direct evidence that Prss53 functions in hair curvature shape and skeletal dysplasia.

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A direct link between Prss53, hair curvature, and skeletal dysplasia

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