Silencing ATG6 and PI3K accelerates petal senescence and reduces flower number and shoot biomass in petunia.

payth.elady61 shared this article with you from Inoreader Silencing ATG6 and PI3K accelerates petal senescence and reduces flower number and shoot biomass in petunia. Via pubmed: autophagy Silencing ATG6 and PI3K accelerates petal senescence and reduces flower number and shoot biomass in petunia. Plant Sci. 2021 Jan;302:110713 Authors: Lin Y, Jones ML Abstract Petal senescence is a form of developmental programmed cell death (PCD) that is regulated by internal and environmental signals. Autophagy, a metabolic pathway that regulates intercellular nutrient recycling, is thought to play an important role in the regulation of petal senescence-associated PCD. To characterize the function of two central autophagy genes in petal senescence, we down-regulated Autophagy Gene 6 (PhATG6) and Phosphoinositide 3-Kinase (PhPI3K) using Virus-Induced Gene Silencing (VIGS) in Petunia × hybrida. The silencing of PhATG6 and PhPI3K accelerated petal senescence, thereby reducing flower longevity. Both PhATG6- and PhPI3K-silenced petunias had reduced flower numbers, flower biomass, and vegetative shoot biomass. These phenotypes were intensified when plants were grown under low nutrient conditions. Additionally, two important regulators of senescence, an ethylene biosynthesis gene (PhACS) and a type I metacaspase gene (PhMC1), were suppressed in senesci ng petals of PhATG6- and PhPI3K-silenced plants. In conclusion, our study identified PhATG6 and PhPI3K as negative regulators of flower senescence and demonstrated the influence of nutrient limitation on the function of autophagy during petal senescence. Our study also found that autophagy genes potentially influence the transcriptional regulation of metacaspases and ethylene biosynthetic genes during petal senescence. The results of this project will be fundamental for future studies of petal senescence and will provide genetic information for future crop improvement. PMID: 33288020 [PubMed - in process] View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.