ArticleDevelopmental cell2022
A cilia-independent function of BBSome mediated by DLK-MAPK signaling in C. elegans photosensation.
Article in Developmental cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- ThebioRxiv : the preprint server for biology · 2026Article
- Neuron-intrinsic and glial pathways regulate sensory cilia regeneration in adultbioRxiv : the preprint server for biology · 2026Article
- Multiple regulators constrain the abundance of Caenorhabditis elegans DLK-1 in ciliated sensory neurons.G3 (Bethesda, Md.) · 2025Article
- Article
- An intraflagellar transport dependent negative feedback regulates the MAPKKK DLK-1 to protect cilia from degeneration.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Organization, functions, and mechanisms of the BBSome in development, ciliopathies, and beyond.eLife · 2023Review
- Article
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Bardet-Biedl syndrome (BBS) is a genetic disorder that affects primary cilia. BBSome, a protein complex composed of eight BBS proteins, regulates the structure and function of cilia, and its malfunction causes BBS in humans. Here, we report a cilia-independent function of BBSome. To identify genes that regulate the C. elegans photoreceptor protein LITE-1 in ciliated ASH photosensory neurons, we performed a genetic screen and isolated bbs mutants. Functional analysis revealed that BBSome regulates LITE-1 protein stability independently of cilia. Through another round of genetic screening, we found that this cilia-independent function of BBSome is mediated by DLK-MAPK signaling, which acts downstream of BBSome to control LITE-1 stability via Rab5-mediated endocytosis. BBSome exerts its function by regulating the expression of DLK. BBSome also regulates the expression of LZK, a mammalian DLK in human cells. These studies identify a cilia-independent function of BBSome and uncover DLK as an evolutionarily conserved BBSome effector.
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