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Its functional defects are associated with infertility and abnormal gametogenesis. However, the specific mechanisms of HELQ in the development of germ cells remain to be elucidated. Here, we uncovered that HELQ deficiency led to proliferation defects of primordial germ cells (PGCs) in mouse embryos, thus compromising the establishment of reproductive reserve. Mechanistically, we found that HELQ interacted with the H3K9me3 demethylase KDM4B, and the absence of HELQ led to a marked increase in both total and chromatin\u2010bound protein levels of KDM4B, resulting in reduced H3K9me3 levels in the region of the retrotransposon LINE\u20101, which triggered its high expression and subsequently caused DNA damage accumulation. Moreover, the developmental defects of HELQ\u2010deficient PGCs were alleviated by inhibition of retrotransposition. These results indicate that HELQ maintains the genome stability of PGCs by repressing LINE\u20101 expression. 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