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The Trihelix Transcription Factor GT2-like 1 (GTL1) promotes salicylic acid metabolism and regulates basal and bacterial effector-triggered Immunity

ABSTRACT: The Trihelix Transcription Factor GT2-like 1 (GTL1) promotes salicylic acid metabolism and regulates basal and bacterial effector-triggered Immunity

PROVIDER: PRJNA486344 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7703201_1.fastq.gz	Fastqsanger.gz
	SRR7703201_2.fastq.gz	Fastqsanger.gz
	SRR7703202_1.fastq.gz	Fastqsanger.gz
	SRR7703202_2.fastq.gz	Fastqsanger.gz
	SRR7703193_1.fastq.gz	Fastqsanger.gz

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The Trihelix Transcription Factor GT2-like 1 (GTL1) promotes salicylic acid metabolism and regulates basal and bacterial effector-triggered Immunity

Project description:We report the transcriptome composition of gtl1-2 compared to Columbia wild-type plant without treatment and after flg22-application

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Root hair specific transcriptome analysis of gain-of-function and loss-of-function of GTL1 and DF1

Project description:How plants determine the final size of growing cells is an important, yet unanswered question. Root hairs provide an excellent model system to study this question since their final cell size is remarkably constant under given environmental conditions. In this study we demonstrate that a trihelix transcription factor GT-2-LIKE1 (GTL1) and its homolog DF1 repress root hair growth in Arabidopsis. Our transcriptional data, combined with genome-wide chromatin binding data, show that GTL1 and DF1 directly bind the RSL4 promoter and regulate its expression to repress root hair growth. Our data further show that GTL1 and RSL4 regulate each other as well as a set of common downstream genes, many of which have previously been implicated in root hair growth. This study therefore uncovers a core regulatory module that fine-tunes the extent of root hair growth by orchestrated actions of opposing transcription factors.

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Transcriptional repression of GTL1 by water-deficit stress promotes anthocyanin and polyamine biosynthesis to enhance drought tolerance

Project description:GT2-LIKE 1 (GTL1) is a negative regulator of stomatal development and its repressed expression under water deficit can result in enhanced drought tolerance. As a transcription factor, GTL1 has been implicated in diverse developmental roles. We hypothesized that GTL1 represses multiple drought tolerance pathways, leading to the drought tolerance phenotype of the gtl1-4 knockout mutant. RNA-Seq data indicates that GTL1 regulates genes involved in ribosome biogenesis in emerging leaves and secondary metabolite synthesis in expanding leaves.

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Project description:We performed a chromatin immunoprecipitation-based microarray experiment (ChIP chip) in order to identify GTL1 and DF1 direct target genes

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The Trihelix transcription factor GT2-like 1 (GTL1) promotes salicylic acid metabolism, and regulates bacterial-triggered immunity.

Project description:The Trihelix Transcription factor GT2-like 1 (GTL1) was previously shown to be a key regulator of ploidy-dependent trichome growth and drought tolerance. Here, we report that GTL1 plays an important role in coordinating plant immunity. We show that gtl1 mutants are compromised in the regulation of basal immunity, microbial pattern-triggered immunity (PTI) and effector-triggered RIN4-mediated immunity. Transcriptome analysis revealed that GTL1 positively regulates defense genes and inhibits factors that mediate growth and development. By performing hormonal measurements and chromatin-immunoprecipitation studies, we found GTL1 to coordinate genes involved in salicylic acid metabolism, transport and response. Interaction studies and comparative transcriptomics to known data sets revealed that GTL1 is part of the MPK4 pathway and regulates oppositely the expression of differentially expressed genes in mpk4 plants. We introduced the gtl1 mutation in the mpk4 mutant and thereby partially suppressed its dwarfism and the high resistance against a bacterial invader. Our data show that GTL1 is part of the MPK4 pathway and acts as a positive regulator of bacterial-triggered immunity and SA homeostasis.

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