Kei‐ichiro Ishiguro

The paper identifies Firrm as a platform coordinating Mcm8-9-Hrob recruitment and Fignl1-mediated Rad51 unloading during homologous recombination.

This study shows that RPA prevents unregulated priming and Rad51 loading on ssDNA in Xenopus egg extracts, maintaining genome stability.

This study shows UTY and UTX work together to maintain gene regulation in human stem cells by supporting transcription factor localization and chromatin accessibility.

The paper shows MEIOSIN has a STRA8-independent activity that drives meiotic entry in vertebrates, with different effects in zebrafish and mice.

This study identifies an Nkx2.3-Nr5a1 gene regulatory axis critical for spleen-specific vascular architecture and marginal zone formation in mice.

This study identifies MAP7 as a key regulator of microtubule remodeling in Sertoli cells, essential for apical domain formation and timely meiotic progression in mouse testes.

The paper shows that Meioc-Piwil1 complexes regulate rRNA transcription in zebrafish spermatogonial stem cells, preventing Piwil1 from localizing to nucleoli and promoting differentiation.

This study identifies HSF5 as a male germ cell-specific factor critical for meiotic prophase progression beyond pachytene under non-stress conditions.

This study identifies ATF7IP2 as a critical regulator of H3K9 methylation and meiotic gene regulation in male germline, showing its role in heterochromatin organization and meiotic sex chromosome inactivation.

This study shows that Mettl1-dependent m7G tRNA modification is essential for spermatogenesis and fertility in Drosophila, as its loss leads to sterility and tRNA instability.

This study identifies MCMBP as essential for MCM2-7 hexamer assembly in human cells, showing its role in DNA replication and its potential as a target for p53-deficient cancers.

This study shows that Trim41 prevents chaotic X chromosome synapsis in male mice, leading to infertility when disrupted.

The paper identifies KCTD19 as essential for meiotic exit in male mice, showing it interacts with ZFP541 and HDAC1, and its deficiency causes apoptosis during meiosis.

This study identifies a ZFP541-KCTD19 repressor complex that promotes meiotic prophase exit in spermatogenesis by suppressing transcriptional regulators and chromatin modifiers.

This study identifies C19orf57 as a factor that modulates RAD51 and DMC1 localization to DSBs during meiotic recombination in mice, impacting DSB repair and male fertility.