Chlorophyllase (PsCLH1) and light-harvesting chlorophyll a/b binding protein 1 (PsLhcb1) and PsLhcb5 maintain petal greenness in Paeonia suffruticosa 'Lv Mu Yin Yu'.

INTRODUCTION: Green flowers are not an adaptive trait in natural plants due to the challenge for pollinators to discriminate from leaves, but they are valuable in horticulture. The molecular mechanisms of green petals remain unclear. Tree peony (Paeonia suffruticosa) is a globally cultivated ornamental plant and considered the 'King of Flowers' in China. The P. suffruticosa 'Lv Mu Yin Yu (LMYY)' cultivar with green petals could be utilized as a representative model for understanding petal-specific chlorophyll (Chl) accumulation and color formation. OBJECTIVES: Identify the key genes related to Chl metabolism and understand the molecular mechanism of petal color changes. METHODS: The petal color parameter was analyzed at five developmental stages using a Chroma Spectrophotometer, and Chl and anthocyanin accumulation patterns were examined. Based on comparative transcriptomes, differentially expressed genes (DEGs) were identified, among which three were functionally characterized through overexpression in tobacco plants or silencing in 'LMYY' petals. RESULTS: During flower development and blooming, flower color changed from green to pale pink, consistent with the Chl and anthocyanin levels. The level of Chl demonstrated a similar pattern with petal epidermal cell striation density. The DEGs responsible for Chl and anthocyanin metabolism were characterized through a comparative transcriptome analysis of flower petals over three critical developmental stages. The key chlorophyllase (PsCLH1) and light-harvesting chlorophyll a/b binding protein 1 (PsLhcb1) and PsLhcb5 influenced the Chl accumulation and the greenness of 'LMYY' petals. CONCLUSION: PsCLH1, PsLhcb1, and PsLhcb5 were critical in accumulating the Chl and maintaining the petal greenness. Flower color changes from green to pale pink were regulated by the homeostasis of Chl degradation and anthocyanin biosynthesis. This study offers insights into underlying molecular mechanisms in the green petal and a strategy for germplasm innovation.

MCT1-mediated transport of valeric acid promotes porcine preimplantation embryo development by improving mitochondrial function and inhibiting the autophagic AMPK-ULK1 pathway.

Oocytes and embryos are highly sensitive to environmental stress in vivo and in vitro. During in vitro culture, many stressful conditions can affect embryo quality and viability, leading to adverse clinical outcomes such as abortion and congenital abnormalities. In this study, we found that valeric acid (VA) increased the mitochondrial membrane potential and ATP content, decreased the level of reactive oxygen species that the mitochondria generate, and thus improved mitochondrial function during early embryonic development in pigs. VA decreased expression of the autophagy-related factors LC3B and BECLIN1. Interestingly, VA inhibited expression of autophagy-associated phosphorylation-adenosine monophosphate-activated protein kinase (p-AMPK), phosphorylation-UNC-51-like autophagy-activated kinase 1 (p-ULK1, Ser555), and ATG13, which reduced apoptosis. Short-chain fatty acids (SCFAs) can signal through G-protein-coupled receptors on the cell membrane or enter the cell directly through transporters. We further show that the monocarboxylate transporter 1 (MCT1) was necessary for the effects of VA on embryo quality, which provides a new molecular perspective of the pathway by which SCFAs affect embryos. Importantly, VA significantly inhibited the AMPK-ULK1 autophagic signaling pathway through MCT1, decreased apoptosis, increased expression of embryonic pluripotency genes, and improved embryo quality.