At the onset of embryogenesis, the segmentation gene network translates maternal inputs into more complex body patterns. Quantitative studies using Drosophila melanogaster embryo as a model have characterized the temporal evolution of the maternal Bicoid (Bcd) gradient as well as downstream hierarchical genes. Nevertheless, how individual cells interpret a dynamic Bcd gradient at different time windows remains elusive. To better understand the temporal readout of Bcd, we developed an optogenetics tool to turn off Bcd transcription activity with blue-light (488nm) illumination while the activity is restored minutes after switching back to dark. We used the hunchback (hb)-MS2 reporter assay to confirm that 488nm illumination immediately abolishes the Bcd-dependent transcription of Hb in the anterior region of the embryo while leaving the posterior Bcd-independent domain intact. By inactivating Bcd activity at different time-windows during the blastoderm stage, we found that Bcd activity during both nuclear cycle (NC) 14 and NC 13 is essential for embryonic viability. Interestingly, although inactivation of Bcd during NC10-12 does not cause embryonic lethality, it results in an anterior shift of the downstream gap genes and pair-rule genes, resembling that of 1-copy Bcd embryos. This suggests that, at early stages, Bcd may be playing a role in presetting the competency of the nuclei to interpret Bcd in the later stages potentially by occupying DNA binding sites and/or remodeling the chromosomal conformation. Furthermore, we analyzed the cuticle patterns of embryos exposed to different time windows of Bcd-inactivation. Even during fast phase of cellularization Bcd inactivation results in embryo lethality, due to subtle defects at the most anterior region (e.g. mouth hook, cirri). Prolonged inactivation of Bcd (throughout cellularization or even earlier) impedes the formation of more posterior structures. This suggests that the more anterior in space the structure is, the later in time cell fate is determined. Last, by combining our optogenetics tool with light-sheet microscopy imaging, we were able to inactivate Bcd activity in only one lateral half of the embryo. We observed that the cephalic furrow formation was blocked at the illuminated side of the embryo, while the tissue invagination occurs normally in the non-illuminated side. As the mechanism of cephalic furrow formation has yet to be understood, our approach has the potential to elucidate the property of this morphological movement and identify essential molecular players. Our future work will focus on understanding the link between the initial Bcd-dependent cell fate determinations and morphogenesis during later embryonic development.