| 研究実績の概要 |
Below is the highlight of our progress in FY2020:
1. In FY2019, we showed that RNAi knockdown of a component of the Spectrin membrane skeleton, alpha-Spectrin, causes delayed in apical dome descent. We have followed up on these preliminary observations and found that adherens junctions are not formed properly in the alpha-Spectrin RNAi embryo. Specifically, in the wild-type embryo the E-Cadherin puncta normally coalesce into more continuous pattern of localization in the junctional region as adherents junctions mature from the initial spot junction like structure to form bell-like adhesive complexes. In the alpha-Spectrin RNAi embryo, E-Cadherin puncta retains spotty appearance for a prolonged period of time. These data suggest a possibility that apical dome fails to descend in the alpha-Spectrin RNAi embryo in part due to defective junctional coalescence. We are in the process of further characterizing this phenotype.
2. To better understand how alpha-Spectrin functions during apical dome descent, we have generated a genomic rescue construct that expresses GFP-tagged alpha-Spectrin. Initial characterization of this construct shows that alpha-Spectrin is highly enriched in the junction region, with additional localization in the apical dome region. Junctional localization of alpha-Spectrin partially overlap with that of E-Cadherin, but is excluded from the tricellular junctional region. We will further characterize the dynamics of this construct and investigate how its localization is regulated.
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