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Updated: Aug 20, 2026

Removal of an Internal Translational Start Site from mRNA While Retaining Expression of the Full-Length Protein
Published on: March 16, 2022
The atspo11-1 mutation rescues atxrcc3 meiotic chromosome fragmentation
Jean-Yves Bleuyard1, Maria E Gallego, Charles I White
1CNRS UMR6547, Université Blaise Pascal, 24, avenue des Landais, Aubière, 63177, France.
Abstract:
Homologous recombination events occurring during meiotic prophase I ensure the proper segregation of homologous chromosomes at the first meiotic division. These events are initiated by programmed double-strand breaks produced by the Spo11 protein and repair of such breaks by homologous recombination requires a strand exchange activity provided by the Rad51 protein. We have recently reported that the absence of AtXrcc3, an Arabidopsis Rad51 paralogue, leads to extensive chromosome fragmentation during meiosis, first visible in diplotene of meiotic prophase I. The present study clearly shows that this fragmentation results from un- or mis-repaired AtSpo11-1 induced double-strand breaks and is thus due to a specific defect in the meiotic recombination process.
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