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Charlotte M. M. Gommers

Researcher at Wageningen University and Research Centre

Publications -  21
Citations -  877

Charlotte M. M. Gommers is an academic researcher from Wageningen University and Research Centre. The author has contributed to research in topics: Shade avoidance & Arabidopsis thaliana. The author has an hindex of 6, co-authored 19 publications receiving 649 citations. Previous affiliations of Charlotte M. M. Gommers include Spanish National Research Council & Utrecht University.

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Shade tolerance: when growing tall is not an option

TL;DR: It is argued that molecular approaches using model and non-model species should help identify the molecular pathways that underpin shade tolerance, thus providing knowledge for further crop improvement.
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Perception of low red:far-red ratio compromises both salicylic acid- and jasmonic acid-dependent pathogen defences in Arabidopsis.

TL;DR: It is shown that both salicylic acid (SA) and jasmonic acid (JA) disease resistance is inhibited by a simultaneously reduced red:far-red light ratio (R:FR), the early warning signal for plant competition.
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Integration of Phytochrome and Cryptochrome Signals Determines Plant Growth during Competition for Light

TL;DR: It is shown in Arabidopsis thaliana that low B in combination with low R:FR enhances petiole elongation similar to vegetation shade, providing functional context for a low B response in plant competition.
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Seedling establishment: A dimmer switch-regulated process between dark and light signaling

TL;DR: A balance between dark and light signaling directs seedling establishment through integrating internal and environmental information.
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Circadian Waves of Transcriptional Repression Shape PIF-Regulated Photoperiod-Responsive Growth in Arabidopsis

TL;DR: The findings provide a framework for recent TIMING of CAB EXPRESSION 1 (TOC1/PRR1) data and reveal that the long described circadian morning-to-midnight waves of the PRR transcriptional repressors jointly gate PIF activity to dawn to prevent overgrowth through sequential regulation of common PIF-PRR target genes such as CDF5.