Protein kinase D is essential for embryonic survival through functionally redundant subtypes
Lei Huang1, Shangbin Cai1, Hong Wang2
1Department of Cardiovascular Surgery, Peking University Shenzhen Hospital, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Peking University, Shenzhen, 518055, China.
Life Sciences
|October 15, 2025
Summary
Protein kinase D (PKD) is essential for mouse embryonic development. Deleting specific PKD gene pairs (Prkd1/Prkd2 or Prkd1/Prkd3) caused severe placental defects and embryonic lethality, highlighting functional redundancy.
Area of Science:
- Molecular Biology
- Developmental Biology
- Genetics
Background:
- Protein kinase D (PKD) is a family of serine/threonine kinases involved in cellular processes like proliferation and apoptosis.
- The precise roles of PKD isoforms during embryonic development are not fully understood.
Purpose of the Study:
- To investigate the impact of deleting Protein kinase D (PKD) genes on embryonic survival and development in mice.
Main Methods:
- Generated single knockout mice for each PKD isoform (Prkd1, Prkd2, Prkd3).
- Created compound double knockout (DKO) models by interbreeding single knockouts.
- Utilized genotypic and histological analyses to assess embryonic viability and morphology.
Main Results:
- Single knockouts of any PKD isoform showed normal embryonic development and survival.
- Deletion of Prkd1 and Prkd2 (DKO1/2) or Prkd1 and Prkd3 (DKO1/3) resulted in severe allantoic-placental defects, leading to embryonic lethality (E10.5-E11.5).
- Deletion of Prkd2 and Prkd3 (DKO2/3) caused later-stage embryonic lethality with partial penetrance and significant growth retardation in survivors.
Conclusions:
- Protein kinase D (PKD) is indispensable for normal embryonic development and survival in mice.
- Distinct PKD isoforms display functional redundancy during embryogenesis.
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