Two related, fully unstructured proteins BASP1 and GAP-43 (neuromodulin) are highly expressed in brain neurons where they participate in axon guidance and synaptic plasticity. Recently, BASP1 was also found to be a critical target of the Sox2 and Myc transcription factors and an inhibitor of iPSCs generation from mouse embryonic fibroblasts. In this study, we have revealed that both BASP1 and GAP-43 proteins are present in mouse oocytes and preimplantation embryos. Using immunocytochemical techniques, BASP1 was found to be localized in the cytoplasm of the oocytes, zygotes and blastomeres, with a more pronounced staining of the plasma membrane and actin cortex. Microinjection of bovine BASP1 into the cytoplasm of the metaphase II (MII) oocytes induced their exit from the MII arrest followed by parthenogenetic embryo development. A possible mechanism of BASP1 participation in oocyte activation may consist in sequestration of the plasma membrane polyphosphoinositides, as studied previously in neurons. GAP-43, which is generally regarded as a marker of the postmitotic neurons, was shown to reside at the meiotic spindle microtubules in the MII oocytes. GAP-43 is also colocalized with γ-tubulin at the spindle poles (centrosomes) and at the discrete microtubule-organizing centers (MTOCs) in the cytoplasm. This is reminiscent of GAP-43 centrosomal association found recently in asymmetrically dividing neuronal progenitors. By analogy to the neuronal progenitors, we suggest that GAP-43 may be involved in regulation of oocyte polarity. GAP-43 was also revealed in blastomere nuclei in preimplantation mouse embryos. Interestingly, distinct blastomeres displayed different expression of GAP-43. Using antibodies to Ser41-phosphorylated form of the protein, GAP-43 was shown to be subject to phosphorylation by protein kinase C in oocytes and blastomeres. The presence of BASP1 and GAP-43 in oocytes was independently confirmed by western blotting and RT-PCR. Our results indicate that the role of BASP1 and GAP-43 in early embryogenesis requires further investigation. Supported by RFBR grant 18-04-01357.