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Slo3 channel is the primary candidate mediating the pH-dependent K+ current (KSper) in mouse sperm.However, because heterologous expression of S1o3 results in currents that are much less activated at physiological conditions that are native KSper currents, the equivalence of Slo3-dependent current and KSper remains uncertain.Here, we show that genetic deletion of Slo3 abolishes all pH-dependent K+ current at physiological membrane potentials in corpus epididymal sperm.At potentials above 0 mV, a residual pH-dependent outward current (IKres) is observed in Slo3-/-sperm.Differential inhibition of KSper/Slo3 and IKres by clofilium reveals that the amplitude of IKres is similar in both wt and Slo3-/-sperm, strongly supporting the idea that IKres is an intrinsic component in native sperm.The properties of IKres suggest that it likely represents outward monovalent cation flux through CatSper channels.Thus, KSper/Slo3 may account for essentially all mouse sperm K+ current and is the sole pH-dependent K+ conductance in these sperm.With deletion of S1o3, the sperm exhibit deficits from distinct aspects, including membrane potential response to alkalization, motility in the absence of bicarbonate, and morphological adaption under hypotonic challenge.As a consequence, Slo3-/-male mice are infertile.Together these results show that KSper/Slo3 is the primary spermatozoan K+ current, which is critical for normal sperm function.