Abstract
Water availability is an important environmental factor that controls flowering time. Many plants accelerate flowering under drought conditions, a phenomenon called drought escape. Four pathways are involved in controlling flowering time, but which ones participate in drought escape is not yet known. In this study, plants with loss-of-function mutations of GIGANTEA (GI) and CONSTANS (CO) exhibited abnormal drought-escape phenotypes. The peak mRNA levels of GI and FKF1 (Flavin-binding Kelch domain F box protein 1) and the mRNA levels of CO and FT (Flowering locus T) changed under drought stress. The microRNA factor miRNA172E was up-regulated by drought stress, and its up-regulation was dependent on GI, while other miRNA172s were not. Water-loss analyses indicated that gi mutants were more sensitive while miRNA172 over-expressing (miRNA172-OX) plants were less so to drought stress than wild-type plants. Digital gene expression and real-time PCR analyses showed that WRKY44 was down-regulated by GI and miRNA172. The WRKY44 protein could interact with TOE1 (a target of miRNA172) in a yeast two-hybrid system. We proposed that GI–miRNA172–WRKY44 may regulate drought escape and drought tolerance by affecting sugar signaling in Arabidopsis.
Highlights
Unlike most animals, plants are sessile organisms
Many terrestrial plants flower earlier when water is deficient, a phenomenon well studied in wheat, Brassica, and Arabidopsis [20,21], but which pathway is involved in drought escape is not yet clear
Because the onset and duration of drought treatment of gi and co was the same as that of wild types (WT) and other plants, these results indicated that the photoperiod pathway might be involved in early flowering under drought
Summary
They cannot move to escape the biotic and abiotic stresses that threaten them throughout their life cycles. Flowering time is regulated by multiple environmental and endogenous factors [4]. These factors can be grouped into four genetic pathways: the photoperiod, phytohormone, vernalization, and autonomous pathways [5,6]. These pathways crosstalk at common targets, such as Flowering Locus T (FT) and Leafy, to promote the transition from vegetative to reproductive phase [4,7]. MiRNA156 inhibits the transcription of miRNA172b via SPL9 and, redundantly, SPL10 [11]
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