The Diabetes Susceptibility Gene Clec16a Regulates Mitophagy
Open accessAbstract
Clec16a has been identified as a disease susceptibility gene for type 1 diabetes, multiple sclerosis, and adrenal dysfunction, but its function is unknown. Here we report that Clec16a is a membrane-associated endosomal protein that interacts with E3 ubiquitin ligase Nrdp1. Loss of Clec16a leads to an increase in the Nrdp1 target Parkin, a master regulator of mitophagy. Islets from mice with pancreas-specific deletion of Clec16a have abnormal mitochondria with reduced oxygen consumption and ATP concentration, both of which are required for normal β cell function. Indeed, pancreatic Clec16a is required for normal glucose-stimulated insulin release. Moreover, patients harboring a diabetogenic SNP in the Clec16a gene have reduced islet Clec16a expression and reduced insulin secretion. Thus, Clec16a controls β cell function and prevents diabetes by controlling mitophagy. This pathway could be targeted for prevention and control of diabetes and may extend to the pathogenesis of other Clec16a- and Parkin-associated diseases.
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We detected no alteration in endoplasmic reticulum morphology in CLEC16A-deficient cells.
“We detected no alteration in endoplasmic reticulum morphology (Fig. 6c), as expected from prior studies of Clec16a-deficient murine islets16.”
From Clec16a is Critical for Autolysosome Function and Purkinje Cell Survival (2016) · cites this paper as [16]
The Results section on pancreas-specific Clec16a deficiency reports that mutant murine β-cells contained large vacuoles likely representing dilated ER, contrary to the cited expectation of unchanged ER morphology in murine islets. The paper reports no noticeably abnormal ER morphology in Clec16a-deficient fibroblasts, but that finding does not apply to the islets named in the citing sentence. (LLM, conf=0.89)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredKnock-down or loss of Clec16a in human and murine cells has been described to alter the morphology of late endosomes.
“Knock-down or loss of Clec16a in human and murine cells has been described to alter the morphology of late endosomes1633 but we did not observe alterations in the endosomal network as detected by staining of endosomes for Rab5, Rab7 or EEA1 in Clec16a-deficient cells (Fig. 5a, Supplementary Fig. 5a).”
From Clec16a is Critical for Autolysosome Function and Purkinje Cell Survival (2016) · cites this paper as [16]
In Results, under “Clec16a is a membrane-associated endolysosomal protein” (page not available), increased Rab7 staining suggests an accumulation of late endosomes after Clec16a loss. Another Results passage describes small vacuoles in deficient mouse β-cells that could be endosomes, but does not establish altered late-endosome morphology. The copy does not report that change in human cells. (LLM, conf=0.85)
Experimental — accuracy not yet measuredReduced fusion has been suggested in studies of mitophagy induction in islet cells lacking Clec16a.
“While in ema-deficient Drosophila cells there is no observed defect in fusion between lysosomes and autophagosomes, reduced fusion has been suggested in studies of mitophagy induction in islet cells lacking Clec16a916.”
From Clec16a is Critical for Autolysosome Function and Purkinje Cell Survival (2016) · cites this paper as [16]
The Results section on late mitophagy reports reduced autophagosome–lysosome marker co-localization after mitophagy induction in Clec16a-deficient fibroblasts, suggesting impaired fusion or trafficking. It also reports autophagic vacuoles and reduced Mfn2 in Clec16a-deficient islets, but the fusion-related measurement was not made in islet cells. No page number is available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe mutations in the gene analyzed here are likely more disruptive of Clec16a function than alleles associated with human disease risk.
“Importantly, the mutations in the gene analyzed here are likely more disruptive of Clec16a function than alleles associated with human disease risk12163342.”
From Clec16a is Critical for Autolysosome Function and Purkinje Cell Survival (2016) · cites this paper as [16]
The Results report that pancreas-specific Clec16a deletion reduced islet transcript by 70%, while the human disease-risk SNP was associated with a dose-dependent decrease in CLEC16A expression. This supports the suggested distinction between a strong experimental disruption and a human risk allele, but the paper does not assess the specific mutations analyzed in the citing document or directly compare their effects with human alleles. No page numbers are available in our copy. (LLM, conf=0.78)
Experimental — accuracy not yet measuredSNPs in CLEC16A associated with autoimmunity may correlate with either increased or decreased CLEC16A protein expression in humans.
“single nucleotide polymorphisms (SNPs) in CLEC16A that are associated with autoimmunity may correlate with either increased or decreased CLEC16A protein expression in humans”
From Clec16a is Critical for Autolysosome Function and Purkinje Cell Survival (2016) · cites this paper as [16]
The Results section on the diabetogenic CLEC16A SNP reports that a type 1 diabetes–associated variant correlates with decreased CLEC16A mRNA in human islets. It does not establish increased expression for any SNP or measure the claimed change in CLEC16A protein expression. (LLM, conf=0.88)
Experimental — accuracy not yet measured
The presence of the diabetes-associated CLEC16A SNP rs12708716 is reported to result in about a two-fold decrease in CLEC16A mRNA expression in human islets.
“the presence of the diabetes-associated CLEC16A SNP rs12708716 is reported to result in about a two-fold decrease in CLEC16A mRNA expression in human islets16.”
From Clec16a is Critical for Autolysosome Function and Purkinje Cell Survival (2016) · cites this paper as [16]
The Results section ('A diabetogenic CLEC16A SNP associated with reduced islet CLEC16A expression and β-cell function in humans'; page unavailable) reports a dose-dependent decrease in CLEC16A mRNA in human islet donors carrying rs12708716. Our copy does not give the claimed approximately two-fold magnitude; it describes an association rather than establishing that the SNP itself causes the decrease. (LLM, conf=0.87)
Experimental — accuracy not yet measuredClec16a-deficient islet cells are reported to exhibit defective insulin secretion in response to glucose challenge.
“Since Clec16a-deficient islet cells are reported to exhibit defective insulin secretion in response to glucose challenge16, we quantified protein secretion using HeLa cells expressing a GFP-tagged FKBP mutant (F36M) linked to human growth hormone (hGH)35.”
From Clec16a is Critical for Autolysosome Function and Purkinje Cell Survival (2016) · cites this paper as [16]
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- Authors
- Soleimanpour, S. A., Gupta, A., Bakay, M., Ferrari, A. M., Groff, D. N., Fadista, J., Spruce, L. A., Kushner, J. A., Groop, L., Seeholzer, S. H., Kaufman, B. A., Hakonarson, H., & Stoffers, D. A.
- Affiliations
- University of Michigan (US)
- University of Pennsylvania (US)
- Children's Hospital of Philadelphia (US)
- Lund University (SE)
- Baylor College of Medicine (US)
- Corresponding author
- Stoffers, Doris A.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2014-06
- Volume
- 157
- Issue
- 7
- Pages
- 1577-1590
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4184276
- OpenAlex
- W2067097574
- Cited by
- 211
- References
- 10
- Citations by year
- 2026: 7 · 2025: 17 · 2024: 19 · 2023: 15 · 2022: 22 · 2021: 22 · 2020: 12 · 2019: 23 · 2018: 12 · 2017: 17 · 2016: 22 · 2015: 20 · 2014: 2 · 2013: 1
- FWCI
- 20.18
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (5-P01-DK-049210-15, K08DK089117, P01DK049210, P30 DK 19525, DP3DK085708, P30DK020572, P30DK019525)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- CLEC16A, mitophagy, Parkin, Nrdp1, type 1 diabetes, beta-cell function, glucose-stimulated insulin secretion, oxygen consumption, ATP production, endosomal proteins, E3 ubiquitin ligase, genetic susceptibility, single nucleotide polymorphisms
- MeSH terms
- Amino Acid Sequence, Animals, Carrier Proteins, Diabetes Mellitus, Type 1, Glucose, Humans, Islets of Langerhans, Lysosomes, Membrane Proteins, Molecular Sequence Data, Monosaccharide Transport Proteins, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Lectins, C-Type, Ubiquitin-Protein Ligases, Insulin-Secreting Cells, Mice, Mitophagy
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