Plays a key role in chromosome recombination and chromosome structure development during meiosis. Required at early steps in meiotic recombination that leads to non-crossovers pathways. Also needed for efficient completion of homologous synapsis by influencing crossover distribution along the chromosomes affecting both crossovers and non-crossovers pathways. Also required for development of higher-order chromosome structures and is needed for synaptonemal-complex formation. In males, required for efficient synapsis of the sex chromosomes and for sex body formation. Promotes early steps of the DNA double-strand breaks (DSBs) repair process upstream of the assembly of RAD51 complexes. Required for depletion of HORMAD1 and HORMAD2 from synapsed chromosomes (PubMed:17696610, PubMed:19851446, PubMed:20711356). Plays a role in mitotic spindle assembly checkpoint (SAC) activation (By similarity). Specifically interacts with the ligand binding domain of the thyroid receptor (TR). This interaction does not require the presence of thyroid hormone for its interaction (By similarity). Interacts with proteasome subunit PSMA8; to participate in meiosis progression during spermatogenesis (PubMed:31437213). Widely expressed, including in testis. Mice develop normally without obvious somatic defects but males and females are sterile due to meiotic disruption in meiocytes. Homozygous mutants display small gonads and females have few or no follicles, due to oocyte elimination between pachynema and dictyate. Mutant testes display reduced populated tubules and spermatogenesis is mainly arrested at spermatocyte stages of epithelial stage IV, corresponding to pachynema. Different phenotypes are observed in the different knockout experiments tested. In Trip13(RRB047) mutant mice, also named Trip13(mod) allele for moderate, the number of crossovers are not affected and meiocytes undergo homologous chromosome synapsis despide the presence of unrepaired DSBs in pachynema. Using a more severe mutant allele, named Trip13(sev) for severe, additional defects are observed: the numbers of crossovers and chiasmata are reduced in the absence of TRIP13, and their distribution along the chromosomes is altered (PubMed:20711356). Autosomal bivalents in meiocytes frequently display pericentric synaptic forks and other defects (PubMed:20711356). Recombination defects are evident very early in meiotic prophase, soon after DSB formation (PubMed:20711356). These results suggest that the absence of defects in the number of crossovers observed in Trip13(RRB047) mutant is due to the use of a weak hypomorphic mutant allele. Belongs to the AAA ATPase family. PCH2 subfamily.