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Biology subjects

Choinard, S.

Publications and source records attributed to Choinard, S..

3 recordsLinked to original sources

Too much sugar makes plants "pregnant": maternal sucrose signals fertilization in Arabidopsis seeds

Reproduction is deemed successful if it ensures the perpetuation of the species. Nonetheless, evolution has optimized reproductive efficiency across a diverse range of strategies. Animal vivipary, the process in which embryos develop inside the parents body, allows for larger offspring and better protection. This reproductive strategy relies on a fertilization signal sent to the maternal tissues to establish an embryo-supportive environment, a process known as "maternal recognition of pregnancy". Despite being a strictly animal-only term, plants independently evolved a conceptually similar strategy: the seed habit, wherein the embryo is nourished and protected by surrounding maternal tissues. We discovered that sucrose is sufficient to trigger a fertilization-independent response in the maternal tissues of Arabidopsis ovules. Upon fertilization, the release of Polycomb-mediated repression promotes the symplastic and apoplastic flow of sucrose into the seed by modulating auxin and trehalose 6-phosphate signaling. The sucrose signal is then perceived by the TARGET OF RAPAMYCIN kinase and transduced into a gibberellin response to initiate the differentiation of the seed maternal tissues. This work revealed a zygotic-maternal interplay of hormonal and sugar signaling that drives the plant "maternal recognition of fertilization", incorporating energetic cues into developmental pathways.

plant biology↗

A change in the cell wall status initiates the elimination of the nucellus in Arabidopsis

The evolution of the seed habit coincides with a change in the cell fate of the nucellus, the sporophytic tissue responsible for female meiosis. Seeds arose when the nucellus retained the female spores instead of releasing them in the environment. As a consequence, the nucellus was partially eliminated to accommodate the growth of the female gametophyte inside the sporophyte. With the evolution of angiosperm seeds, the process of nucellus elimination was requisitioned to allow the growth of the endosperm, the second fertilization product devoted to store nutrients. Cell elimination differs from most known cell death programs as it leads to the apparent dismantling of the cell wall. Here, we show that nucellus elimination in Arabidopsis is initiated by the lysis of the pectic polysaccharides in the cell wall. This process exposes other cell wall components to possible further degradation and precedes a cell death program that leads to nuclear DNA fragmentation. Both pathways are regulated by TRANSPARENT TESTA 16, a MADS-domain transcription factor that evolved with seed plants. Finally, the causal effect of cell wall modification on nucellus development is demonstrated by inhibiting pectin degradation, thus suggesting that a change in the cell wall status might have driven seed evolution.

plant biology↗

FIGL1 and its novel partner FLIP form a conserved complex that regulates homologous recombination.

Homologous recombination is central to repair DNA double-strand breaks (DSB), either accidently arising in mitotic cells or in a programed manner at meiosis. Crossovers resulting from the repair of meiotic breaks are essential for proper chromosome segregation and increase genetic diversity of the progeny. However, mechanisms regulating CO formation remain elusive. Here, we identified through protein-protein interaction and genetic screens FIDGETIN-LIKE-1 INTERACTING PROTEIN (FLIP) as a new partner of the previously characterized anti-crossover factor FIDGETIN-LIKE-1 (FIGL1) in Arabidopsis thaliana. We showed that FLIP limits meiotic crossover together with FIGL1. Further, FLIP and FIGL1 form a protein complex conserved from Arabidopsis to Human. FIGL1 interacts with the recombinases RAD51 and DMC1, the enzymes that catalyze the DNA stand exchange step of homologous recombination. Arabidopsis flip mutants recapitulates the figl1 phenotype, with enhanced meiotic recombination associated with change in DMC1 dynamics. Our data thus suggest that FLIP and FIGL1 form a conserved complex that regulates the crucial step of strand invasion in homologous recombination.

genetics↗