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Ana M. López

Researcher at University of Sheffield

Publications -  12
Citations -  477

Ana M. López is an academic researcher from University of Sheffield. The author has contributed to research in topics: DNA methylation & Arabidopsis thaliana. The author has an hindex of 7, co-authored 12 publications receiving 390 citations. Previous affiliations of Ana M. López include Polytechnic University of Valencia & Spanish National Research Council.

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Plant perception of β-aminobutyric acid is mediated by an aspartyl-tRNA synthetase

TL;DR: A mutant of Arabidopsis thaliana is described that is impaired in BABA-induced disease immunity (ibi1) but hypersensitive to BA BA-induced growth repression, which opens new opportunities to separate broad-spectrum disease resistance from the associated costs on plant growth.
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An extracellular subtilase switch for immune priming in Arabidopsis.

TL;DR: The identified an extracellular subtilase from Arabidopsis, SBT3.3, the overexpression of which enhances innate immune responses while the loss of function compromises them, and points to an epigenetic control in the regulation of plant immunity.
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Role of NPR1 and KYP in long-lasting induced resistance by β-aminobutyric acid

TL;DR: The mechanistic basis of long-lasting induced resistance after treatment with β -aminobutyric acid (BABA), an agent that mimics biologically induced resistance phenomena, is investigated and it is proposed that KYP enables long-term defense gene priming by silencing suppressor genes of SA/NPR1-dependent genes.
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Mediated Plastid RNA Editing in Plant Immunity

TL;DR: The Arabidopsis nuclear-encoded homeodomain-containing protein OCP3 is incorporated into the chloroplast, and contributes to control over the extent of ndhB transcript editing, and rapid destabilization of the plastidial NDH complex is observed in the plant following perception of a pathogenic cue.
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The relationship between transgenerational acquired resistance and global DNA methylation in Arabidopsis.

TL;DR: The study has shown that the Arabidopsis epigenome responds globally to disease in previous generations and its contribution to TAR, and it is revealed that ancestral disease stress preferentially acts on methylation-labile cytosine positions, but also extends tomethylation-stable positions.