Publication Information
Waterworth et al., 2019
Abstract
Plant J. 2019 Dec;100(5):1007-1021. doi: 10.1111/tpj.14495. Epub 2019 Sep 10.
Phosphoproteomic analysis reveals plant DNA damage signalling pathways with a
functional role for histone H2AX phosphorylation in plant growth under genotoxic
stress.
Waterworth WM(1), Wilson M(1), Wang D(2), Nuhse T(3), Warward S(3), Selley J(3),
West CE(1).
Author information:
(1)Centre for Plant Sciences, University of Leeds, Woodhouse Lane, Leeds, LS2
9JT, UK.
(2)Leeds Omics, University of Leeds, Leeds, LS2 9JT, UK.
(3)Faculty of Life Sciences, University of Manchester, Oxford Road, Manchester,
M13 9PT, UK.
DNA damage responses are crucial for plant growth under genotoxic stress.
Accumulating evidence indicates that DNA damage responses differ between plant
cell types. Here, quantitative shotgun phosphoproteomics provided
high-throughput analysis of the DNA damage response network in callus cells. MS
analysis revealed a wide network of highly dynamic changes in the phosphoprotein
profile of genotoxin-treated cells, largely mediated by the ATAXIA
TELANGIECTASIA MUTATED (ATM) protein kinase, representing candidate factors that
modulate plant growth, development and DNA repair. A C-terminal dual serine
target motif unique to H2AX in the plant lineage showed 171-fold phosphorylation
that was absent in atm mutant lines. The physiological significance of
post-translational DNA damage signalling to plant growth and survival was
demonstrated using reverse genetics and complementation studies of h2ax mutants,
establishing the functional role of ATM-mediated histone modification in plant
growth under genotoxic stress. Our findings demonstrate the complexity and
functional significance of post-translational DNA damage signalling responses in
plants and establish the requirement of H2AX phosphorylation for plant survival
under genotoxic stress.
© 2019 The Authors. The Plant Journal published by Society for Experimental
Biology and John Wiley & Sons Ltd.
DOI: 10.1111/tpj.14495
PMCID: PMC6900162
PMID: 31410901 [Indexed for MEDLINE]
Conflict of interest statement: The authors have no conflict of interest to
declare.
