Structure-function analysis of Cdc25Twine degradation at the Drosophila maternal-to-zygotic transition
Patrick L Ferree1, Maggie Xing1, Jenny Q Zhang2
1Department of Cell Biology, Duke University Medical Center, Durham, NC, USA.
Downregulation of protein phosphatase Cdc25Twine activity is linked to remodelling of the cell cycle during the Drosophila maternal-to-zygotic transition (MZT). Here, we present a structure-function analysis of Cdc25Twine. We use chimeras to show that the N-terminus regions of Cdc25Twine and Cdc25String control their differential degradation dynamics. Deletion of different regions of Cdc25Twine reveals a putative domain involved in and required for its rapid degradation during the MZT. Notably, a very similar domain is present in Cdc25String and deletion of the DNA replication checkpoint results in similar dynamics of degradation of both Cdc25String and Cdc25Twine. Finally, we show that Cdc25Twine degradation is delayed in embryos lacking the left arm of chromosome III. Thus, we propose a model for the differential regulation of Cdc25 at the Drosophila MZT.
Downregulation of protein phosphatase Cdc25Twine activity is linked to remodelling of the cell cycle during the Drosophila maternal-to-zygotic transition (MZT). Here, we present a structure-function analysis of Cdc25Twine. We use chimeras to show that the N-terminus regions of Cdc25Twine and Cdc25String control their differential degradation dynamics. Deletion of different regions of Cdc25Twine reveals a putative domain involved in and required for its rapid degradation during the MZT. Notably, a very similar domain is present in Cdc25String and deletion of the DNA replication checkpoint results in similar dynamics of degradation of both Cdc25String and Cdc25Twine. Finally, we show that Cdc25Twine degradation is delayed in embryos lacking the left arm of chromosome III. Thus, we propose a model for the differential regulation of Cdc25 at the Drosophila MZT.
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