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Related Experiment Video

Updated: Jul 22, 2026

Imaging Centrosomes in Fly Testes

Imaging Centrosomes in Fly Testes

Published on: September 20, 2013

SAK/PLK4 is required for centriole duplication and flagella development.

M Bettencourt-Dias¹, A Rodrigues-Martins, L Carpenter

¹Cancer Research UK Cell Cycle Genetics Research Group, Department of Genetics, University of Cambridge, Downing Street, Cambridge CB2 3EH, United Kingdom. mbcd2@cam.ac.uk

Current Biology : CB

|December 6, 2005

Summary

SAK/PLK4 is essential for centriole duplication in both fruit flies and humans. Loss of SAK/PLK4 prevents centriole formation, leading to mitotic defects and impacting sperm development and flagella assembly.

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Area of Science:

Cell Biology
Molecular Biology
Genetics

Background:

SAK/PLK4 is a polo-like kinase family member.
SAK-/- mice exhibit embryonic lethality.
SAK+/- mice and MEFs display tumor development and mitotic abnormalities, respectively, with unknown mechanisms.

Purpose of the Study:

Investigate the mechanism underlying SAK/PLK4-related phenotypes.
Determine the role of SAK/PLK4 in centriole duplication.
Elucidate the function of SAK/PLK4 in cell division and development.

Main Methods:

RNA interference (RNAi) and gene mutation in Drosophila cells.
Analysis of mitotic spindle poles and centriole integrity.
Mathematical modeling of spermatogenesis cell divisions.
Depletion of SAK in human cells.

Main Results:

SAK/PLK4 downregulation causes loss of centrioles in Drosophila cells.
SAK mutants exhibit defective centriole duplication during male meiosis, impacting spermatid development.
SAK depletion in human cells also prevents centriole duplication and causes mitotic abnormalities.

Conclusions:

SAK/PLK4 is crucial for centriole duplication in both Drosophila and human cells.
Drosophila cells lacking centrioles can divide but fail to form basal bodies and flagella.
SAK depletion in human cells leads to error-prone mitosis, suggesting a tumor-suppressor role.