Interestingly, inhibition of store-operated Ca2+ entry in mouse oocytes using pharmacological agents, or by preventing STIM1-Orai1 interaction through the expression of specific protein fragments, does not prevent the sperm-induced Ca2+ oscillations (Miao et al. 2012; Takahashi et al. 2013). This implies that mouse oocytes apply a Ca2+ entry mechanism other than that controlled by the intracellular store to maintain Ca2+ oscillations at fertilization. As mentioned above, the Ca2+ influx in the mouse seems to be under the control of PKC. A candidate channel to provide Ca2+ influx at fertilization is the transient receptor potential (TRP) channel. The TRP protein serves as a Ca2+ channel in a number of cell types and is expressed in various oocytes (Petersen et al. 1995; Machaty et al. 2002). Certain TRP isoforms are known to be regulated by PKC (Hardie 2007), which would account for the stimulatory effect of PKC on the sperm-induced Ca2+ signal. However, recent research has indicated that the TRP channel is not required for normal fertilization (Carvacho et al. 2013). Stimulation of TRPV3 channels leads to Ca2+ entry and subsequent oocyte activation but oocytes collected from transgenic mice that lack TRPV3 channels are able to generate the repetitive Ca2+ spikes characteristic of normal fertilization. This shows that TRPV3 is not essential to sustain the regenerative Ca2+ signal and thus the identity of the Ca2+ entry mechanism that operates in mouse oocytes at fertilization is still unclear.
Devader activation code and serial number
2ff7e9595c
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