Context-specific TE control is crucial to preserve the integrity of the host genome. Repression of TEs is particularly important during gametogenesis, as mutations would be transmitted to the next generation and would compromise the fitness of the progeny. The fetal stages of gametogenesis are characterized by an extensive erasure of DNA methylation, leading to a transient relaxation of the chromatin that could result in derepression and mobilization of TEs. To avoid such threat, DNA methylation is rapidly reestablished by the action of specialized de novo DNA methyltransferases and maintained after birth during spermatogenesis and in the mature spermatozoa. Meiosis is an important process during spermatogenesis, in which haploid cells are generated and homologous recombination causes genetic exchange between homologs. Chromatin organization is highly dynamic during early meiosis and plays a critical role in meiotic progression. It has been previously shown that failure to methylate young TEs during fetal gametogenesis leads to reactivation of young TEs. It is not immediately detrimental but causes damage after birth: meiotic chromosome pairing is altered, leading to apoptosis and male sterility. We aim at deciphering the mechanisms driving this developmental arrest, using two mouse models of TE reactivation: a) Deficient DNA methylation using DNMT3C-KO; or b) Temporally controlled CRISPR-based activation. We will 1) investigate the impact of TE activity on meiotic chromatin landscape and distribution of recombination sites, and meiotic chromosome conformation and 2) control TE reactivation in space and time to assess the impact of different TE subfamilies. Based on previous findings, we hypothesize that meiotic arrest is not due to retrotransposition, but hypomethylated young TEs acquire a relaxed chromatin environment that attracts the meiotic HR machinery, leading to synaptic failure and non-homologous recombination. Additionally, TE reactivation could impact neighboring genes, leading to aberrant transcriptional activation at a stage otherwise characterized by transcriptional shutdown.