Physiological function of seminal vesicle secretions on male fecundity

Noda, T, Ikawa, M. Physiological function of seminal vesicle secretions on male fecundity. Reprod Med Biol. 2019; 18: 241– 246. https://doi.org/10.1002/rmb2.1228

GPI-AP release in cellular, developmental, and reproductive biology

Yoshitaka Fujihara, Masahito Ikawa, GPI-AP release in cellular, developmental, and reproductive biology, Journal of Lipid Research, Volume 57, Issue 4, 2016, Pages 538-545, ISSN 0022-2275, https://doi.org/10.1194/jlr.R063032

Mouse spermatozoa with higher fertilization rates have thinner nuclei

Mashiko D, Ikawa M, Fujimoto K. 2017. Mouse spermatozoa with higher fertilization rates have thinner nuclei. PeerJ 5:e3913 https://doi.org/10.7717/peerj.391

The mechanics clarifying counterclockwise rotation in most IVF eggs in mice

Ishimoto, K., Ikawa, M. & Okabe, M. The mechanics clarifying counterclockwise rotation in most IVF eggs in mice. Sci Rep 7, 43456 (2017). https://doi.org/10.1038/srep4345

The mechanism of sperm-egg interaction and the involvement of IZUMO1 in fusion

Inoue, N., Ikawa, M., & Okabe, M. (2011). The mechanism of sperm-egg interaction and the involvement of IZUMO1 in fusion. Asian Journal of Andrology, 13(1), 81-87. doi:10.1038/aja.2010.7

Putative sperm fusion protein IZUMO and the role of N-glycosylation

IZUMO is the mouse sperm protein proven to be essential for fusion with eggs. It contains one immuno- globulin-like domain with a conserved glycosylation site within. In the present paper, we produced trans- genic mouse lines expressing unglycosylated IZUMO (N204Q-IZUMO) in Izumo1 / background. The expression of N204Q-IZUMO rescued the infertile phenotype of IZUMO disrupted mice, indicating glyco- sylation is not essential for fusion-facilitating activity of IZUMO. The N204Q-IZUMO was produced in tes- tis in comparable amounts to wild-type IZUMO, but the amount of N204Q-IZUMO on sperm was significantly decreased by the time sperm reached the cauda epididymis. These data suggest that glyco- sylation is not essential for the function of IZUMO, but has a role in protecting it from fragmentation in cauda epididymis

Gene-deficient mouse model established by CRISPR/Cas9 system reveals 15 reproductive organ-enriched genes dispensable for male fertility

Since the advent of gene-targeting technology in embryonic stem cells, mice have become a primary model organism for investigating human gene function due to the striking genomic similarities between the two species. With the introduction of the CRISPR/Cas9 system for genome editing in mice, the pace of loss-of-function analysis has accelerated significantly. This has led to the identification of numerous genes that play crucial roles in male reproductive processes, including meiosis, chromatin condensation, flagellum formation in the testis, sperm maturation in the epididymis, and fertilization in the oviduct. Despite the advancements, the functions of many genes, particularly those enriched in male reproductive tissues, remain largely unknown. In our study, we focused on 15 genes and generated 13 gene-deficient mice [4933411K16Rik, Adam triple (Adam20, Adam25, and Adam39), BC048671, Cfap68, Gm4846, Gm4984, Gm13570, Nt5c1b, Ppp1r42, Saxo4, Sh3d21, Spz1, and Tektl1] to elucidate their roles in male fertility. Surprisingly, all 13 gene-deficient mice exhibited normal fertility in natural breeding experiments, indicating that these genes are not essential for male fertility. These findings have important implications as they may help prevent other research laboratories from duplicating efforts to generate knockout mice for genes that do not demonstrate an apparent phenotype related to male fertility. By shedding light on the dispensability of these genes, our study contributes to a more efficient allocation of research resources in the exploration of male reproductive biology

Generation of Hprt-disrupted rat through mouse← rat ES chimeras

Isotani, A., Yamagata, K., Okabe, M. et al. Generation of Hprt-disrupted rat through mouse←rat ES chimeras. Sci Rep 6, 24215 (2016). https://doi.org/10.1038/srep2421

Mice expressing aberrant sperm-specific protein PMIS2 produce normal-looking but fertilization-incompetent spermatozoa

Yamaguchi, R., Fujiharaa, Y., Ikawa, M., & Okabe, M. (2012). Mice expressing aberrant sperm-specific protein PMIS2 produce normal-looking but fertilization-incompetent spermatozoa. Molecular Biology of the Cell, 23(14), 2671-2679. doi:10.1091/mbc.E11-12-102