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Phosphoinositides are a group of phospholipids containing a glycerol backbone with two fatty acid chains and a phosphate attached to a myoinositol sugar ring. The inositol head group extends into the cytoplasm, where it is modified by adding phosphate groups to form phosphatidylinositol phosphates or PIPs.
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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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Updated: Jul 15, 2025

Single-molecule Super-resolution Imaging of Phosphatidylinositol 4,5-bisphosphate in the Plasma Membrane with Novel Fluorescent Probes
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The signalling lipid PI3,5P2 is essential for timely mitotic exit.

Mariam Huda1, Seyma Nur Bektas1, Baris Bekdas1

  • 1Department of Molecular Biology and Genetics, Koç University, Istanbul, Turkey.

Open Biology
|September 26, 2023
PubMed
Summary

Phosphatidylinositol-3,5-bisphosphate (PI3,5P2) regulates mitotic exit timing in yeast. This lipid signaling molecule impacts the spindle position checkpoint, influencing cell division progression.

Keywords:
PI3mitosismitotic exitmitotic exit networkphosphoinositidesignalling lipid

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Successful mitosis requires precise coordination between chromosome segregation and mitotic exit.
  • The mitotic exit network (MEN) controls mitotic exit in budding yeast, with the spindle position checkpoint (SPOC) providing negative regulation.
  • SPOC kinase Kin4 is essential for activating the SPOC pathway in response to spindle mispositioning.

Purpose of the Study:

  • To investigate the role of phosphatidylinositol-3,5-bisphosphate (PI3,5P2) in regulating the timing of mitotic exit.
  • To elucidate the mechanism by which PI3,5P2 influences mitotic exit and its relationship with the SPOC pathway.

Main Methods:

  • Yeast genetics to manipulate PI3,5P2 levels and study mitotic phenotypes.
  • Analysis of mitotic exit timing in cells with altered PI3,5P2 signaling.
  • Investigating the interaction between PI3,5P2, Kin4, and the effector protein Atg18.

Main Results:

  • Absence of PI3,5P2 leads to delayed mitotic exit.
  • Elevated PI3,5P2 levels accelerate mitotic exit in cells with defects.
  • PI3,5P2 promotes mitotic exit by impairing Kin4 activity, a process dependent on Atg18.

Conclusions:

  • PI3,5P2 plays a novel and critical role in controlling the timing of mitotic exit.
  • A new regulatory link is established between PI3,5P2 signaling and the spindle position checkpoint.
  • This finding expands our understanding of cell cycle regulation and lipid signaling pathways.