Sperm transport in the female genital tract is physiologically important for mammalian fertilization. The female reproductive system contains multiple natural selective barriers, such as successful uterotubal junction (UTJ) migration and zona pellucida (ZP) binding, to ensure sperm with normal motility and morphology to transmit into oviduct for fertilization (Yanagimachi, 1994; Ikawa et al., 2010). Tex101 is a glycosylphosphatidyl inositol (GPI)-anchored glycoprotein identified as a molecular marker of germ cells (Kurita et al., 2001). Although there have been indications that the malfunction of Tex101 may affect male fertility (Yin et al., 2009), little is known about its exact physiological function and the underlying molecular mechanisms. Recently, a study showed that Tex101 gene knockout sperm were unable to pass through UTJ or bind to ZP, which led to male infertility (Fujihara et al., 2013). Here, we independently generated Tex101 knockout mice and confirmed the infertile phenotype caused by UTJ migration defect. We also found that Tex101 knockout sperm lost the adhesive ability to the surface of female genital tract. Several members of a disintegrin and metalloprotease (ADAM) transmembrane protein family with cell adhesion ability, including ADAM3, ADAM4, ADAM5, and ADAM6, were lost in Tex101 knockout epididymal sperm. These observations may shed new light on the diagnosis of male infertility and development of contraceptive methods in human.