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Aluminum-induced terminal differentiation in Arabidopsis roots requires the stem cell niche transcription factor ETHYLENE RESPONSE FACTOR 115

ABSTRACT: Aluminum-induced terminal differentiation in Arabidopsis roots requires the stem cell niche transcription factor ETHYLENE RESPONSE FACTOR 115

PROVIDER: PRJNA919037 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22999800_1.fastq.gz	Fastqsanger.gz
	SRR22999800_2.fastq.gz	Fastqsanger.gz
	SRR22999801_1.fastq.gz	Fastqsanger.gz
	SRR22999801_2.fastq.gz	Fastqsanger.gz
	SRR22999802_1.fastq.gz	Fastqsanger.gz

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Aluminum-induced terminal differentiation in Arabidopsis roots requires the stem cell niche transcription factor ETHYLENE RESPONSE FACTOR 115

Project description:Aluminum-dependent stoppage of root growth and terminal differentiation depend on a functional DNA damage response pathway comprised of the master cell cycle checkpoint ATR (ATAXIA TELANGIECTASIA-MUTATED AND RAD3-RELATED) and p53-like transcription factor SOG1 (SUPPRESSOR OF GAMMA RADIATION 1). Mutational loss of either results in failure to trigger endoreduplication following Al treatment even in the Al-hypersensitive mutant, als3-1. Transcriptome analyses were used to identify several Al-induced SOG1-regulated targets as candidate mediators of Al-dependent growth arrest including SMR5, SMR7, ERF114 and ERF115. Analysis of these factors either as loss-of-function/silenced mutants or by overexpression in the als3-1 background indicates ERF115, a key transcription factor involved in stem cell niche restoration, is important for the switch from an actively growing root to one that has terminally differentiated. Consistent with this, a putative ERF115 ortholog and other DDR factors from barley are also upregulated following Al exposure, suggesting a conserved role for this ATR-dependent pathway in response to Al. In contrast to other ts show that ERF115 and related family members are important determinants for the switch to endoreduplication in the root tip following Al exposure and a central output of the ATR-mediated pathway in Al response.

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Project description:Gene expression profiling in soybean under aluminum stress: mechanisms of magnesium amelioration of aluminum toxicity at gene expression level. Micro-molar concentrations of magnesium in culture solution has been shown to ameliorate Al toxicity in soybean and other leguminous species. Different theories have been proposed to explain the chemical mechanisms of how the two ions interact to neutralize the toxic effect of aluminum in the plant root system. To understand the molecular mechanisms of the phenomenon at the gene expression level in soybean, we undertook a comparative transcriptome analysis in Al-tolerant and Al-sensitive genotypes treated with aluminum alone or aluminum plus magnesium using DNA microarrays. The results revealed magnesium enhances Al-tolerance level in the Al-tolerant genotype by down-regulating genes commonly induced in response to Al toxicity. We hypothesized that the magnesium-mediated alleviation of Al toxicity in the Al-tolerant genotype emanates from reduction in energy expenditure of gene expression induced in response to Al stress. Conversely, magnesium appears to ameliorate Al toxicity in the sensitive genotype by dual mechanisms of increasing the expression level of several genes involved in Al-tolerance and decreasing the expression level of most genes. Keywords: Soybean, aluminum toxicity, magnesium, transcriptome

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