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  1. ; ; ; ; ; ; ; ; ; ; et al ( , Journal of Experimental Botany)
    Abstract

    Anthocyanins and proanthocyanins (PAs) are two end products of the flavonoid biosynthesis pathway. They are believed to be synthesized in the endoplasmic reticulum and then sequestered into the vacuole. In Arabidopsis thaliana, TRANSPARENT TESTA 19 (TT19) is necessary for both anthocyanin and PA accumulation. Here, we found that MtGSTF7, a homolog of AtTT19, is essential for anthocyanin accumulation but not required for PA accumulation in Medicago truncatula. MtGSTF7 was induced by the anthocyanin regulator LEGUME ANTHOCYANIN PRODUCTION 1 (LAP1), and its tissue expression pattern correlated with anthocyanin deposition in M. truncatula. Tnt1-insertional mutants of MtGSTF7 lost anthocyanin accumulation in vegetative organs, and introducing a genomic fragment of MtGSTF7 could complement the mutant phenotypes. Additionally, the accumulation of anthocyanins induced by LAP1 was significantly reduced in mtgstf7 mutants. Yeast-one-hybridization and dual-luciferase reporter assays revealed that LAP1 could bind to the MtGSTF7 promoter to activate its expression. Ectopic expression of MtGSTF7 in tt19 mutants could rescue their anthocyanin deficiency, but not their PA defect. Furthermore, PA accumulation was not affected in the mtgstf7 mutants. Taken together, our results show that the mechanism of anthocyanin and PA accumulation in M. truncatula is different from that in A. thaliana, and provide a new target gene for engineering anthocyanins in plants.

     
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  2. ; ; ; ; ; ; ; ; ; ; et al ( , New Phytologist)
    Summary

    In species with compound leaves, the positions of leaflet primordium initiation are associated with local peaks of auxin accumulation. However, the role of auxin during the late developmental stages and outgrowth of compound leaves remains largely unknown.

    Using genome resequencing approaches, we identified insertion sites at four alleles of theLATERAL LEAFLET SUPPRESSION1(LLS1) gene, encoding the auxin biosynthetic enzyme YUCCA1 inMedicago truncatula.

    Linkage analysis and complementation tests showed that thells1mutant phenotypes were caused by theTnt1insertions that disrupted theLLS1gene. The transcripts ofLLS1can be detected in primordia at early stages of leaf initiation and later in the basal regions of leaflets, and finally in vein tissues at late leaf developmental stages. Vein numbers and auxin content are reduced in thells1‐1mutant. Analysis of thells1 sgl1andlls1 palm1double mutants revealed thatSGL1is epistatic toLLS1, andLLS1works withPALM1in an independent pathway to regulate the growth of lateral leaflets.

    Our work demonstrates that the YUCCA1/YUCCA4 subgroup plays very important roles in the outgrowth of lateral leaflets during compound leaf development ofM. truncatula, in addition to leaf venation.

     
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