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Vahisalu, T.

Publications and source records attributed to Vahisalu, T..

2 recordsLinked to original sources

The EGY1-SGR1 module controls chloroplast development and senescence by modulating photosynthetic functions

The chloroplast plays essential roles not only in production of biochemical energy and metabolism, but also in plant development, including senescence. We describe a mutant with an unusual progression of senescence and identify it as an allele of ethylene-dependent gravitropism-deficient and yellow-green 1 (egy1-5). EGY1 encodes a chloroplast-localized metalloprotease that regulates chlorophyll metabolism. The single egy1-5 mutant exhibits defects in various aspects of chloroplast function, including abnormal accumulation of photosynthetic complexes, defects in photosynthetic electron transfer chain and altered responses to the chemicals methyl viologen and lincomycin. Additionally, egy1 lacks guard cell chloroplasts. We performed a suppressor mutant screen in the egy1 background to identify new regulators of senescence and chloroplast development. We found two suppressors that restored green leaves and mapping revealed that both suppressors had mutations in STAY-GREEN 1 (SGR1). SGR1 encodes the Mg2+ dechelatase enzyme, which catalyses the first step in chlorophyll breakdown. Several defects in the egy1 mutant were either fully or partially suppressed in egy1 sgr1. This enabled the function of EGY1 to be isolated, independent of the pleiotropic effects of chlorophyll degradation. Our findings suggest that chlorophyll homeostasis regulates the overall development and function of the chloroplast as well as plant senescence. HighlightIdentifying new mutants with defects in chlorophyll metabolism and chloroplast development shows that proper chlorophyll homeostasis is necessary for maintaining functional chloroplasts.

plant biology↗

Genetic screen to saturate guard cell signaling network reveals a role of GDP-L-fucose metabolism in stomatal closure

Guard cells regulate plant gas exchange by controlling the aperture of stomatal pores. The process of stomatal closure involves a multi-input signaling network that governs the activity of ion channels, which in turn regulate guard cell turgor pressure and volume. Here we describe a forward genetic screen to identify novel components involved in stomatal movements. Through an ozone-sensitivity approach combined with whole-rosette gas exchange analysis, 130 mutants of established stomatal regulators and 76 novel mutants impaired in stomatal closure were identified. One of the novel mutants was mapped to MURUS1 (MUR1), the first enzyme in de novo GDP-L-fucose biosynthesis. Defects in synthesis or import of GDP-L-Fuc into the Golgi apparatus resulted in impaired stomatal closure to multiple stimuli. Stomatal phenotypes observed in mur1 were independent from the canonical guard cell signaling and instead could be related to altered mechanical properties of guard cell walls. Impaired fucosylation of xyloglucan, N-linked glycans and arabinogalactan proteins did not explain the aberrant function of mur1 stomata, however our data suggest that the stomatal phenotypes observed in mur1 can at least partially be attributed to defective dimerization of rhamnogalactouronan-II. In addition to providing the genetic framework for future studies on guard cell signaling, our work emphasizes the impact of fucose metabolism on stomatal movement.

plant biology↗