Functions of Sphingolipids in Pathogenesis During Host-Pathogen Interactions.

Sphingolipids are a class of membrane lipids that serve as vital structural and signaling bioactive molecules in organisms ranging from yeast to animals. Recent studies have emphasized the importance of sphingolipids as signaling molecules in the development and pathogenicity of microbial pathogens including bacteria, fungi, and viruses. In particular, sphingolipids play key roles in regulating the delicate balance between microbes and hosts during microbial pathogenesis. Some pathogens, such as bacteria and viruses, harness host sphingolipids to promote development and infection, whereas sphingolipids from both the host and pathogen are involved in fungus-host interactions. Moreover, a regulatory role for sphingolipids has been described, but their effects on host physiology and metabolism remain to be elucidated. Here, we summarize the current state of knowledge about the roles of sphingolipids in pathogenesis and interactions with host factors, including how sphingolipids modify pathogen and host metabolism with a focus on pathogenesis regulators and relevant metabolic enzymes. In addition, we discuss emerging perspectives on targeting sphingolipids that function in host-microbe interactions as new therapeutic strategies for infectious diseases.

The Arabidopsis KH-domain protein FLOWERING LOCUS Y delays flowering by upregulating FLOWERING LOCUS C family members.

KEY MESSAGE: We identified FLY as a previously uncharacterized RNA-binding-family protein that controls flowering time by positively regulating the expression of FLC clade members. The ability of flowering plants to adjust the timing of the floral transition based on endogenous and environmental signals contributes to their adaptive success. In Arabidopsis thaliana, the MADS-domain protein FLOWERING LOCUS C (FLC) and the FLC clade members FLOWERING LOCUS M/MADS AFFECTING FLOWERING1 (FLM/MAF1), MAF2, MAF3, MAF4, and MAF5 form nuclear complexes that repress flowering under noninductive conditions. However, how FLM/MAF genes are regulated requires further study. Using a genetic strategy, we showed that the previously uncharacterized K-homology (KH) domain protein FLOWERING LOCUS Y (FLY) modulates flowering time. The fly-1 knockout mutant and FLY artificial microRNA knockdown line flowered earlier than the wild type under long- and short-day conditions. The knockout fly-1 allele, a SALK T-DNA insertion mutant, contains an ~ 110-kb genomic deletion induced by T-DNA integration. FLC clade members were downregulated in the fly-1 mutants and FLY artificial microRNA knockdown line, whereas the level of the FLC antisense transcript COOLAIR was similar to that of the wild type. Our results identify FLY as a regulator that affects flowering time through upregulation of FLC clade members.