Multiple genetic pathways act in response to developmental cues and environmental signals to promote the floral transition, by regulating several floral pathway integrators. These include FLOWERING LOCUS T (FT) and SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 (SOC1). We show that the flowering repressor SHORT VEGETATIVE PHASE (SVP) is controlled by the autonomous, thermosensory, and gibberellin pathways, and directly represses SOC1 transcription in the shoot apex and leaf. Moreover, FT expression in the leaf is also modulated by SVP. SVP protein associates with the promoter regions of SOC1 and FT, where another potent repressor FLOWERING LOCUS C (FLC) binds. SVP consistently interacts with FLC in vivo during vegetative growth and their function is mutually dependent. Our findings suggest that SVP is another central regulator of the flowering regulatory network, and that the interaction between SVP and FLC mediated by various flowering genetic pathways governs the integration of flowering signals.

Background-Abnormal host-microbe interactions are implicated in the pathogenesis of inflammatory bowel diseases. Previous 16S rRNA sequence analysis of intestinal tissues demonstrated that a subset of Crohn's disease (CD) and ulcerative colitis (UC) samples exhibited altered intestinal associated microbial compositions characterized by depletion of Bacteroidetes and Firmicutes (particularly Clostridium taxa). We hypothesize that NOD2 and ATG16L1 risk

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