98%
921
2 minutes
20
Heterotrimeric G-proteins influence almost all aspects of plant growth, development, and responses to biotic and abiotic stresses in plants, likely via their interaction with specific effectors. However, the identity of such effectors and their mechanism of action are mostly unknown. While investigating the roles of different G-protein subunits in modulating the oil content in Camelina (), an oil seed crop, we uncovered a role of Gβ proteins in controlling anisotropic cell expansion. Knockdown of genes causes reduced longitudinal and enhanced transverse expansion, resulting in altered cell, tissue, and organ shapes in transgenic plants during vegetative and reproductive development. These plants also exhibited substantial changes in their fatty acid and phospholipid profiles, which possibly leads to the increased oil content of the transgenic seeds. This increase is potentially caused by the direct interaction of Gβ proteins with a specific patatin-like phospholipase, pPLAIIIδ. Camelina plants with suppressed expression exhibit higher lipase activity, and show phenotypes similar to plants overexpressing , suggesting that the Gβ proteins are negative regulators of pPLAIIIδ. These results reveal interactions between the G-protein-mediated and lipid signaling/metabolic pathways, where specific phospholipases may act as effectors that control key developmental and environmental responses of plants.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6393804 | PMC |
http://dx.doi.org/10.1104/pp.18.01312 | DOI Listing |
Animals (Basel)
July 2024
Department of Animal Science, College of Animal Science, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
Guanidinoacetic acid (GAA) can effectively improve the metabolism of energy and proteins by stimulating creatine biosynthesis. We present a study exploring the impact of GAA on production performance, serum biochemistry, meat quality and rumen fermentation in Hu sheep. A total of 144 weaned male Hu sheep (body weight 16.
View Article and Find Full Text PDFEur J Hum Genet
March 2021
Department of Pediatrics, Erasmus MC University Medical Center, Rotterdam, The Netherlands.
Pompe disease is a lysosomal and neuromuscular disorder caused by deficiency of acid alpha-glucosidase (GAA), and causes classic infantile, childhood onset, or adulthood onset phenotypes. The biochemical diagnosis is based on GAA activity assays in dried blood spots, leukocytes, or fibroblasts. Diagnosis can be complicated by the existence of pseudodeficiencies, i.
View Article and Find Full Text PDFFish Shellfish Immunol
February 2020
Clinical Pathology Department, Faculty of Veterinary Medicine, Mansoura University, Mansoura, 35516, Egypt.
A total of 180 unsexed Nile Tilapia fish (initial weight, 21 g) fed isonitrogenous (32%), isocaloric (3000 kcal/kg) diets containing different levels of guanidinoacetic acid (GAA) at levels of (GAA1, 0.06%, GAA2, 0.12%, GAA3, 0.
View Article and Find Full Text PDFPLoS One
May 2019
Bruce Lefroy Centre for Genetic Health Research, Murdoch Children's Research Institute, Parkville, Victoria, Australia.
Background: Friedreich ataxia (FRDA) is an autosomal recessive neurodegenerative condition which also has effects on the heart. In 96% of affected individuals FRDA is due to homozygosity of a GAA repeat expansion in intron 1 of the frataxin (FXN) gene. The number of GAA repeats have been shown to relate to disease severity in FRDA, this thought to be via an inverse relationship of GAA repeat number and cellular frataxin levels.
View Article and Find Full Text PDFPLoS One
March 2011
Department of Neurological Sciences, University Federico II, Naples, Italy.
Background: Friedreich's ataxia (FRDA) is the most common hereditary ataxia among caucasians. The molecular defect in FRDA is the trinucleotide GAA expansion in the first intron of the FXN gene, which encodes frataxin. No studies have yet reported frataxin protein and mRNA levels in a large cohort of FRDA patients, carriers and controls.
View Article and Find Full Text PDF