Modification of maternally defined H3K4me3 regulates the inviability of interspecific Xenopus hybrids

Increasing evidence suggests that interspecific hybridization is crucial to speciation. However, chromatin incom-patibility during interspecific hybridization often renders this process. Genomic imbalances such as chromo-somal DNA loss and rearrangements leading to infertility have been commonly noted in hybrids. The mechanism underlying reproductive isolation of interspecific hybridization remains elusive. Here, we identified that modification of maternally defined H3K4me3 in Xenopus laevis and Xenopus tropicalis hybrids determines the different fates of the two types of hybrids as texls with developmental arrest and viable lexts. Transcrip-tomics highlighted that the P53 pathway was overactivated, and the Wnt signaling pathway was suppressed in texls hybrids. Moreover, the lack of maternal H3K4me3 in texls disturbed the balance of gene expression between the L and S subgenomes in this hybrid. Attenuation of p53 can postpone the arrested development of texls. Our study suggests an additional model of reproductive isolation based on modifications of maternally defined H3K4me3. Commons

Automated summary

Increasing evidence shows that interspecific hybridization plays a crucial role in speciation, but chromatin compatibility issues often hinder this process. Genomic imbalances, such as chromosomal DNA loss and rearrangements, lead to infertility in hybrids. The mechanism behind reproductive isolation in interspecific hybridization remains unknown. In this study, it was found that the modification of maternally defined H3K4me3 in Xenopus laevis and Xenopus tropicalis hybrids determines the fate of the hybrids, with texls showing developmental arrest and lexts being viable. Transcriptomic analysis revealed that the P53 pathway is overactivated and the Wnt signaling pathway is suppressed in texls hybrids. Furthermore, the lack of maternal H3K4me3 disrupts gene expression balance between the L and S subgenomes in texls hybrids. Attenuation of p53 can delay the arrested development of texls. This study proposes an additional model of reproductive isolation based on modifications of maternally defined H3K4me3.