CIQUIBIC   05472
CENTRO DE INVESTIGACIONES EN QUIMICA BIOLOGICA DE CORDOBA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
The DNA glycosylase AtMBD4L controls FLC expression and flowering time in Arabidopsis thaliana.
Autor/es:
IGNACIO LESCANO; MARÍA ELENA ÁLVAREZ; FLORENCIA NOTA
Lugar:
virtual
Reunión:
Congreso; LVI SAIB Meeting - XV SAMIGE Meeting; 2020
Resumen:
Flowering is a complex process regulated by developmental, hormonal and environmental cues that operate through different pathways. The Flowering Locus C (FLC) encodes a MADS box-like transcription factor that negatively regulates flowering-associated genes. FLC repression triggers flowering, and is controlled by changes in epigenetic marks of the locus signaled by the autonomous pathway or the expression of antisense RNAs (COOLAIR) induced by vernalization. To date the regulation of flowering time by DNA glycosylases has not been described. DNA glycosylases excise and replace damaged bases from DNA, acting at initial stages of the base excision DNA repair system, and some of these enzymes may affect chromatin structure. In this work, we studied the role of the DNA glycosylase MBD4L (methyl-binding domain protein 4 like) on flowering time regulation in Arabidopsis thaliana. MBD4L mutants (mbd4l) flowered earlier than WT (wild-type) plants, and this phenotype was rescued by the overexpression of MBD4L. mbd4l early flowering was observed at both short and long day conditions, without significant changes in the expression of flowering activator CONSTANS. Therefore, MBD4L may regulate flowering independently of photoperiod. Interestingly, a strong downregulation of FLC was observed at early developmental stages of mbd4l mutants. To identify the possible pathways that lead to this phenotype, we analyzed the transcript levels of spliced and unspliced FLC, COOLAIR, and other related genes such as FRIGIDA, SOC1 and FT. Our results suggest that MBD4L is a novel component acting in a different pathway of the flowering signaling network, possibly through epigenetic mechanisms.