Dataset Information

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

ABSTRACT: 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.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE222336 | GEO | 2024/08/27

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:Aluminum (Al) toxicity and phosphate (Pi) limitation are widespread chronic abiotic and mutually enhancing stresses that profoundly affect crop yield. Both stresses causes a strong inhibition of root growth due to a progressive exhaustion of the stem cell niche. Here we report on a CASEIN KINASE 2 (CK2) inhibitor identified by its capability to maintain a functional root stem cell niche under Al toxic conditions. CK2 operates through phosphorylation of the cell cycle checkpoint activator SUPPRESSOR OF GAMMA RADIATION 1 (SOG1), priming its activity under DNA damaging conditions. In addition to yielding Al tolerance, both CK2 and SOG1 inactivation result in resistance to phosphate starvation, revealing the existence of a low phosphate induced cell cycle checkpoint that depends on the DNA damage activator ATAXIA-TELANGIECTASIA MUTATED (ATM). Overall, our data reveal an important physiological role for the plant DNA damage response pathway under agricultural limiting growth conditions and opening new avenues to cope with the problem of Pi limitation. SOG1 can be phosphorylated by both ATM and ATR (Sjogren et al., 2015; Yoshiyama et al., 2017). ATM phosphorylation of SOG1 can occur at five different S/TQ sites upon treatment with double-stand break inducing compounds such as zeocin. This phosphorylation is important for its activity, as demonstrated by the inability of a phosphor-mutant allele to complement the sog1 mutant. In addition to the ATM/ATR-dependent phosphorylation sites, 11 putative CK2 phosphorylation sites [T/SXXE/D, with S or T serving as the phospho-acceptor site (Meggio and Pinna, 2003)] are found within the full length SOG1 proteins. Among these, four sites are conserved among orthologous proteins, stressing their potential importance to protein function. Of these, three cluster at the extreme C-terminus of SOG1, which also is also the location of the ATM/ATR phosphorylation sites. To test putative phosphorylation of any of these sites, TAP-tagged SOG1 protein was extracted and purified from cell cultures and subjected to phosphorylation analysis.

Project description:Background Ionic aluminum (mainly Al3+) is rhizotoxic and can be present in acid soils at concentrations high enough to inhibit root growth. Many forest tree species grow naturally in acid soils and often tolerate high concentrations of Al. Previously, we have shown that aspen (Populus tremula) releases citrate and oxalate from roots in response to Al exposure. To obtain further insights into the root responses of aspen to Al, we investigated root gene expression at Al conditions that inhibit root growth. Results Treatment of the aspen roots with 500 µM Al induced a strong inhibition of root growth within 6 h of exposure time. The root growth subsequently recovered, reaching growth rates comparable to that of control plants. Changes in gene expression were determined after 6 h, 2 d, and 10 d of Al exposure. Replicated transcriptome analyses using the Affymetrix poplar genome array revealed a total of 175 significantly up-regulated and 69 down-regulated genes, of which 70% could be annotated based on Arabidopsis genome resources. Between 6 h and 2 d, the number of responsive genes strongly decreased from 202 to 26, and then the number of changes remained low. The responses after 6 h were characterized by genes involved in cell wall modification, ion transport, and oxidative stress. Two genes with prolonged induction were closely related to the Arabidopsis Al tolerance genes ALS3 (for Al sensitive 3) and MATE (for multidrug and toxin efflux protein, mediating citrate efflux). Patterns of expression in different plant organs and in response to Al indicated that the two aspen genes are homologs of the Arabidopsis ALS3 and MATE. Conclusion Exposure of aspen roots to Al results in a rapid inhibition of root growth and a large change in root gene expression. The subsequent root growth recovery and the concomitant reduction in the number of responsive genes presumably reflect the success of the roots in activating Al tolerance mechanisms. The aspen genes ALS3 and MATE may be important components of these mechanisms.

Dataset Information

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

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets