1,721,016 research outputs found
Select Ahead : Interaction Technique to Improve Efficiency of Object Selection in Virtual Environment with 3D Cursor
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An interactive region-annotation method for specifying and assessing anatomical regions on 3D human organ models
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ISOLATION OF HIGHER CROSSOVER RATE MUTANTS IN ARABIDOPSIS
No full textMeiotic recombination produces crossovers from SPO11-mediated DSBs by diverse interhomolog
repair pathways. The crossovers affect genetic diversity in population and breeding. Crossover is
limited to ~1-3 along a chromosome by three distinct anti-crossover pathways that include FANCM,
RECQ4 and FIGL1 factors in Arabidopsis. However, the mechanism underlying crossover suppression
in which the DSBs (~40-50 per chromosome) are repaired to 1-3 crossovers remains explored clearly.
We have performed high throughput genetic screenings of higher crossover rate (hcr) mutants by using
fluorescent seed-based system, enabling the measurement of crossover frequency in individual plants
of various mutant pools. Three hcr mutants (hcr1, hcr2, hcr3) were isolated and confirmed to be new
anti-crossover mutants by genetic analyses and crossover measurements. The isolation and
characterization of hcr mutants reveal new anti-crossover pathways, providing an insight into the
crossover suppression mechanism in plants.1
High throughput genetic screening of higher crossover rate mutants in Arabidopsis
No full textMeiotic homologous recombination generates crossovers from programmed DSBs via
interhomolog repair pathways. The meiotic crossover frequency and distribution affect genetic
diversity in population and breeding. Crossover number is restricted to ~1-3 along a
chromosome by anti-crossover factors including FANCM, RECQ4 and FIGL1 in Arabidopsis.
However, the mechanism how the excessive DSBs (~40-50 per chromosome) are repaired to
only 1-3 crossovers remains further elucidated. We performed a high throughput genetic
screening of higher crossover rate (hcr) mutants by using fluorescent seed-based system,
enabling the measurement of crossover frequency in individual plants from EMS-driven mutant
pool. We have isolated three hcr mutants (hcr1, hcr2, hcr3) that were confirmed to be new anticrossover
mutants by genetic analysis and deep-sequencing. In this poster we will present
characterization of hcr2 and hcr3 mutants, including mapping of them and their effects on
crossover frequency.1
Differentiated function and localisation of SPO11-1 and PRD3 on the chromosome axis during meiotic DSB formation in Arabidopsis thaliana.
Get PDFDuring meiosis, DNA double-strand breaks (DSBs) occur throughout the genome, a subset of which are repaired to form reciprocal crossovers between chromosomes. Crossovers are essential to ensure balanced chromosome segregation and to create new combinations of genetic variation. Meiotic DSBs are formed by a topoisomerase-VI-like complex, containing catalytic (e.g. SPO11) proteins and auxiliary (e.g. PRD3) proteins. Meiotic DSBs are formed in chromatin loops tethered to a linear chromosome axis, but the interrelationship between DSB-promoting factors and the axis is not fully understood. Here, we study the localisation of SPO11-1 and PRD3 during meiosis, and investigate their respective functions in relation to the chromosome axis. Using immunocytogenetics, we observed that the localisation of SPO11-1 overlaps relatively weakly with the chromosome axis and RAD51, a marker of meiotic DSBs, and that SPO11-1 recruitment to chromatin is genetically independent of the axis. In contrast, PRD3 localisation correlates more strongly with RAD51 and the chromosome axis. This indicates that PRD3 likely forms a functional link between SPO11-1 and the chromosome axis to promote meiotic DSB formation. We also uncovered a new function of SPO11-1 in the nucleation of the synaptonemal complex protein ZYP1. We demonstrate that chromosome co-alignment associated with ZYP1 deposition can occur in the absence of DSBs, and is dependent on SPO11-1, but not PRD3. Lastly, we show that the progression of meiosis is influenced by the presence of aberrant chromosomal connections, but not by the absence of DSBs or synapsis. Altogether, our study provides mechanistic insights into the control of meiotic DSB formation and reveals diverse functional interactions between SPO11-1, PRD3 and the chromosome axis
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