Lithium-induced ciliary lengthening sparks Arp2/3 complex-dependent endocytosis.

Area of Science:

• Cell Biology
• Molecular Biology
• Biochemistry

Background:

• Ciliary length is tightly regulated but can be altered by external factors like lithium.
• Lithium exposure leads to ciliary elongation in various cell types and organisms.
• The precise mechanism of lithium-induced ciliary elongation remains unclear.

Purpose of the Study:

• To investigate the molecular mechanism underlying lithium-induced ciliary elongation in *Chlamydomonas reinhardtii*.
• To determine the role of protein synthesis and membrane dynamics in this process.
• To identify the cellular pathways involved in supplying membrane to elongating cilia.

Main Methods:

• Utilized the alga *Chlamydomonas reinhardtii* as a model system.
• Applied brefeldin and dynasore treatments to assess membrane trafficking.
• Perturbed endocytosis pathways using genetic and chemical methods targeting Arp2/3 complex and dynamin.
• Analyzed actin filament formation near the ciliary base.

Main Results:

• Protein synthesis is not required for lithium-induced ciliary elongation.
• Membrane supply for elongation originates from the cell surface via endocytosis, not the Golgi apparatus.
• Inhibition of endocytosis (Arp2/3 complex, dynamin) blocks lithium-mediated ciliary lengthening.
• Lithium treatment increases actin filaments associated with the endocytic pathway at the ciliary base.

Conclusions:

• Lithium induces ciliary elongation by enhancing endocytic membrane supply, independent of protein synthesis.
• The Arp2/3 complex and dynamin-dependent endocytosis are crucial for this process.
• The endocytic pathway serves as a conserved mechanism for ciliary membrane supply.