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Clathrin-independent endocytosis

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Overview

Clathrin-independent carriers (CLICs) are prevalent tubulovesicular membranes responsible for non-clathrin mediated endocytic events. They appear to endocytose material into GPI-anchored protein-enriched early endosomal compartment (GEECs). Collectively, CLICs and GEECs comprise the Cdc42-mediated CLIC/GEEC endocytic pathway, which is regulated by GRAF1.[1][2][3]

While clathrin-coasted endocytosis is the most efficient means of cellular entry, endocytic pathways can operate without the presence of the clathrin triskelion. In the absence of clathrin, there are many elements of response that allow for the internalization of essential molecules to cellular function.

Mechanisms of Clathrin-independent carriers

Fast Endophilin-Mediated Endocytosis

Fast endophilin-mediated endocytosis is a form of clathrin-independent endocytosis uses cargo capture by cytolytic proteins to allow for endophilin and receptor endocytosis.[4]

CLIC/GEEC Endocytic Pathway

Figure 1: Clathrin-independent endocytic processes uses (a) FEME, (b) CLIC/GEEC, and (c) CL-Lect hypothesis

Crescent shaped tubular clathrin-independent carriers (CLICs) mature into glycosylphosphatidylinositol (GPI)-anchored protein-enriched early endocytic compartments(GEECs)[5].

Role of Glycolipid-Lectin

Glycolipid-lectin, of the galectin family, facilitate tubular endocytic pits drive CLIC/GEEC endocytosis. Glycolipid-lectin binds onto cargo via a carbohydrate, and oligomerizes. This oligomerization allows the Glycolipid-lectin-protein-cargo complex to interact with glycosphingolipid(GSL)-binding subunits and causes a bending of the membrane. [4]. Proteins like galectin-3, galectin 8, and GSL-dependent cellular endocytosis of CD166 are all known to use Glycolipid-lectin.

References

  1. ^ Lundmark, R.; Doherty, G.J.; Howes, M.T.; et al. (November 2008). "The GTPase-Activating Protein GRAF1 Regulates the CLIC/GEEC Endocytic Pathway". Current Biology. 18 (22): 1802–8. doi:10.1016/j.cub.2008.10.044. PMC 2726289. PMID 19036340.
  2. ^ Rossatti, P.; Ziegler, L.; Schregle, R; et al. (November 2019). "Cdc42 Couples T Cell Receptor Endocytosis to GRAF1-Mediated Tubular Invaginations of the Plasma Membrane". Cells. 8 (11): 1388. doi:10.3390/cells8111388. PMC 6912536. PMID 31690048.
  3. ^ Elkin, S.R.; Lakoduk, A.M.; Schmid, S.L. (May 2016). "Endocytic pathways and endosomal trafficking: a primer". Wiener Medizinische Wochenschrift. 166 (7–8): 196–204. doi:10.1007/s10354-016-0432-7. PMC 4873410. PMID 26861668.
  4. ^ Ferreira, Antonio P.A.; Boucrot, Emmanuel (2018-03). "Mechanisms of Carrier Formation during Clathrin-Independent Endocytosis". Trends in Cell Biology. 28 (3): 188–200. doi:10.1016/j.tcb.2017.11.004. ISSN 0962-8924. {{cite journal}}: Check date values in: |date= (help)
  5. ^ Shafaq-Zadah, Massiullah; Dransart, Estelle; Johannes, Ludger (2020-8). "Clathrin-independent endocytosis, retrograde trafficking, and cell polarity". Current Opinion in Cell Biology. 65: 112–121. doi:10.1016/j.ceb.2020.05.009. ISSN 0955-0674. PMC 7588825. PMID 32688213. {{cite journal}}: Check date values in: |date= (help)