GSE134989
RNA-seq analysis in syp-2::AID and N2 controls with and without auxin treatment (4 hours at 4 mM concentration)
Chromosome movements and programmed DNA double-strand breaks (DSBs) promote homologue pairing and initiate recombination at meiosis onset. Checkpoints implement termination of these events when all chromosomes achieve synapsis and form crossover precursors, ensuring meiotic progression. We show that termination of chromosome movement and DSB formation is reversible and is continuously implemented by the synaptonemal complex (SC), which silences chromosome signals that promote CHK-2 activity. Forced removal of the SC or different meiosis-specific cohesin complexes, which are individually required for SC stability, causes rapid CHK-2-dependent reinstallation of the DSB-formation and chromosome-movement machinery. This nuclear reorganization occurs without transcriptional changes, but requires signalling from HORMA protein HTP-1. Conversely, CHK-2 inactivation causes rapid disassembly of the DSB-formation and chromosome-movement machinery. Thus, nuclear organization is constantly controlled by the level of CHK-2 activity. Our results uncover an unexpected plasticity of the meiotic program and show how chromosome signalling integrates nuclear organization with meiotic progression. Overall design: 4 samples in quadruplicate: N2-wo (WT control); N2-IAA (N2 with auxin treatment); S-wo (syp-2::AID worms without auxin treatment); S-IAA (syp-2::AID worms with auxin treatment)