Abstract
ABSTRACTTheFLOWERING LOCUS T(FT)gene is the essential integrator of flowering regulatory pathways in angiosperms. The paralogs of theFTgene may perform antagonistic functions, as exemplified byBvFT1, that suppresses flowering inBeta vulgaris, unlike the paralogous activatorBvFT2. The roles ofFTgenes in other amaranths were less investigated. Here, we transformedArabidopsis thalianawith theFLOWERING LOCUS T like(FTL) genes ofChenopodiumand found, that bothFTL1andFTL2-1accelerated flowering, despite having been the homologs of theBeta vulgarisfloral promoter and suppressor, respectively. The floral promotive effect ofFTL2-1was so strong that it caused lethality when overexpressed under the35Spromoter.FTL2-1placed in inducible cassette accelerated flowering after the induction with methoxyphenozide. The occasional expression ofFTL2-1led to precocious flowering in some primary transformants even without chemical induction. After theFTLgene duplication in Amaranthaceae, theFTL1copy maintained the role of floral activator. The second copyFTL2underwent subsequent duplication and functional diversification, which enabled to control the onset of flowering in amaranths to adapt to variable environments.HIGHLIGHTTheFLOWERING LOCUS T like 2-1(FTL 2-1) gene ofChenopodiumacts as a strong activator of flowering in Arabidopsis, despite being a homolog of floral repressorBvFT1.
Publisher
Cold Spring Harbor Laboratory