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A multi-level response to DNA damage induced by aluminium.

ABSTRACT: Aluminium (Al) ions are one of the primary growth-limiting factors for plants on acid soils, globally restricting agriculture. Despite its impact, little is known about Al action in planta. Earlier work has indicated that, among other effects, Al induces DNA damage. However, the loss of major DNA damage response regulators, such SOG1, partially suppressed the growth reduction in plants seen on Al-containing media. This raised the question whether Al actually causes DNA damage and, if so, how. Here, we provide cytological and genetic data corroborating that exposure to Al leads to DNA double-strand breaks. We find that the Al-induced damage specifically involves homology-dependent (HR) recombination repair. Using an Al toxicity assay that delivers higher Al concentrations than used in previous tests, we find that sog1 mutants become highly sensitive to Al. This indicates a multi-level response to Al-induced DNA damage in plants.

SUBMITTER: Chen P

PROVIDER: S-EPMC6850279 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature

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A multi-level response to DNA damage induced by aluminium.

Chen Poyu P Sjogren Caroline A CA Larsen Paul B PB Schnittger Arp A

The Plant journal : for cell and molecular biology 20190301 3

Aluminium (Al) ions are one of the primary growth-limiting factors for plants on acid soils, globally restricting agriculture. Despite its impact, little is known about Al action in planta. Earlier work has indicated that, among other effects, Al induces DNA damage. However, the loss of major DNA damage response regulators, such SOG1, partially suppressed the growth reduction in plants seen on Al-containing media. This raised the question whether Al actually causes DNA damage and, if so, how. He ...[more]

PMID: 30657222

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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:Radiation induced bystander effects are an important component of the overall response of cells to irradiation and are associated with human health risks. The mechanism responsible includes intra-cellular and inter-cellular signaling by which the bystander response is propagated. However, details of the signaling mechanism are not well defined.We measured the bystander response of Mrad9+/+ and Mrad9-/- mouse embryonic stem cells, as well as human H1299 cells with inherent or RNA interference-mediated reduced RAD9 levels after exposure to 1 Gy ? particles, by scoring chromosomal aberrations and micronuclei formation, respectively. In addition, we used microarray gene expression analyses to profile the transcriptome of directly irradiated and bystander H1299 cells.We demonstrated that Mrad9 null enhances chromatid aberration frequency induced by radiation in bystander mouse embryonic stem cells. In addition, we found that H1299 cells with reduced RAD9 protein levels showed a higher frequency of radiation induced bystander micronuclei formation, compared with parental cells containing inherent levels of RAD9. The enhanced bystander response in human cells was associated with a unique transcriptomic profile. In unirradiated cells, RAD9 reduction broadly affected stress response pathways at the mRNA level; there was reduction in transcript levels corresponding to genes encoding multiple members of the UVA-MAPK and p38MAPK families, such as STAT1 and PARP1, suggesting that these signaling mechanisms may not function optimally when RAD9 is reduced. Using network analysis, we found that differential activation of the SP1 and NUPR1 transcriptional regulators was predicted in directly irradiated and bystander H1299 cells. Transcription factor prediction analysis also implied that HIF1? (Hypoxia induced factor 1 alpha) activation by protein stabilization in irradiated cells could be a negative predictor of the bystander response, suggesting that local hypoxic stress experienced by cells directly exposed to radiation may influence whether or not they will elicit a bystander response in neighboring cells.

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A multi-level response to DNA damage induced by aluminium.

Publications

A multi-level response to DNA damage induced by aluminium.

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