ArticlePLoS biology2011
Hyperactive neuroendocrine secretion causes size, feeding, and metabolic defects of C. elegans Bardet-Biedl syndrome mutants.
Article in PLoS biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- Double mutation of open syntaxin and UNC-18 P334A leads to excitatory-inhibitory imbalance and impairs multiple aspects ofbioRxiv : the preprint server for biology · 2023Article
- A cilia-independent function of BBSome mediated by DLK-MAPK signaling in C. elegans photosensation.Developmental cell · 2022Article
- ROS and cGMP signaling modulate persistent escape from hypoxia in Caenorhabditis elegans.PLoS biology · 2022Article
- Sexual morph specialisation in a trioecious nematode balances opposing selective forces.Scientific reports · 2022Article
- Impairing one sensory modality enhances another by reconfiguring peptidergic signalling ineLife · 2022Article
- Primary Cilia in Pancreatic β- and α-Cells: Time to Revisit the Role of Insulin-Degrading Enzyme.Frontiers in endocrinology · 2022Review
- Temperature regulates synaptic subcellular specificity mediated by inhibitory glutamate signaling.PLoS genetics · 2021Article
- ENPL-1, theDevelopment (Cambridge, England) · 2020Article
- Global Transcriptome Changes That Accompany Alterations in Serotonin Levels inG3 (Bethesda, Md.) · 2020Article
- Bardet-Biedl Syndrome Caused by Skipping of SCLT1 Complicated by Microvesicular Steatohepatitis.Internal medicine (Tokyo, Japan) · 2020Article
- Primary Cilium, An Unsung Hero in Maintaining Functional β-cell Population.The Yale journal of biology and medicine · 2019Review
- Trafficking of ciliary membrane proteins by the intraflagellar transport/BBSome machinery.Essays in biochemistry · 2018Review
- Kynurenic acid accumulation underlies learning and memory impairment associated with aging.Genes & development · 2018Article
- From phenologs to silent suppressors: Identifying potential therapeutic targets for human disease.Molecular reproduction and development · 2017Review
- UNC-18 and Tomosyn Antagonistically Control Synaptic Vesicle Priming Downstream of UNC-13 inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Investigating Connections between Metabolism, Longevity, and Behavior in Caenorhabditis elegans.Trends in endocrinology and metabolism: TEM · 2016Review
- Whole organism transcriptome analysis of zebrafish models of Bardet-Biedl Syndrome and Alström Syndrome provides mechanistic insight into shared and divergent phenotypes.BMC genomics · 2016Article
- C. elegans Body Cavity Neurons Are Homeostatic Sensors that Integrate Fluctuations in Oxygen Availability and Internal Nutrient Reserves.Cell reports · 2016Article
- Differential effects on β-cell mass by disruption of Bardet-Biedl syndrome or Alstrom syndrome genes.Human molecular genetics · 2016Article
- Cell-cycle quiescence maintains Caenorhabditis elegans germline stem cells independent of GLP-1/Notch.eLife · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Bardet-Biedl syndrome, BBS, is a rare autosomal recessive disorder with clinical presentations including polydactyly, retinopathy, hyperphagia, obesity, short stature, cognitive impairment, and developmental delays. Disruptions of BBS proteins in a variety of organisms impair cilia formation and function and the multi-organ defects of BBS have been attributed to deficiencies in various cilia-associated signaling pathways. In C. elegans, bbs genes are expressed exclusively in the sixty ciliated sensory neurons of these animals and bbs mutants exhibit sensory defects as well as body size, feeding, and metabolic abnormalities. Here we show that in contrast to many other cilia-defective mutants, C. elegans bbs mutants exhibit increased release of dense-core vesicles and organism-wide phenotypes associated with enhanced activities of insulin, neuropeptide, and biogenic amine signaling pathways. We show that the altered body size, feeding, and metabolic abnormalities of bbs mutants can be corrected to wild-type levels by abrogating the enhanced secretion of dense-core vesicles without concomitant correction of ciliary defects. These findings expand the role of BBS proteins to the regulation of dense-core-vesicle exocytosis and suggest that some features of Bardet-Biedl Syndrome may be caused by excessive neuroendocrine secretion.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.