# A tale of Rabs and the exocyst complex in ciliary trafficking and biogenesis

**Authors:** Priyanka Upadhyai, Debalina Bose, Neha Quadri

PMC · DOI: 10.3389/fcell.2025.1574638 · 2025-05-06

## TL;DR

This paper reviews how Rabs and the exocyst complex regulate protein transport to the primary cilium, impacting its formation and function.

## Contribution

The paper integrates findings on Rab and exocyst roles in ciliary trafficking and links their dysfunction to ciliopathies.

## Key findings

- Rab and Rab-like proteins regulate transport to the primary cilium.
- The exocyst complex is involved in ciliary biogenesis and function.
- Dysfunction in Rabs or exocyst is linked to ciliopathy-like phenotypes.

## Abstract

The primary cilium is a microtubule-based sensory cell organelle templated by a modified parent centriole that mediates mechanotransduction and response to biochemical cues such as morphogens to regulate organismal development and homeostasis. Given that the cilium is a specialized microdomain devoid of its translation machinery, it relies on the endomembrane pathway for the delivery of proteins and other biomolecules to it. This review provides a comprehensive insight into how membrane trafficking modulators such as Rab and Rab-like proteins, and the exocyst complex control transport to the primary cilia, in turn regulating various aspects of their assembly and function. We integrate findings from in vitro and animal models and draw on human diseases associated with the dysfunction of Rabs or exocyst that exhibit phenotypes overlapping with those of ciliopathies, which further support their relevance to cilia biogenesis and maintenance.

## Linked entities

- **Proteins:** AGFG1 (ArfGAP with FG repeats 1)
- **Diseases:** ciliopathies (MONDO:0005308)

## Full-text entities

- **Genes:** AGFG1 (ArfGAP with FG repeats 1) [NCBI Gene 3267] {aka HRB, RAB, RIP}
- **Diseases:** ciliopathies (MESH:D000072661)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12089063/full.md

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Source: https://tomesphere.com/paper/PMC12089063