ArticlePLoS genetics2020
Control of clathrin-mediated endocytosis by NIMA family kinases.
Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- PIKI-1, a class II PI 3-kinase, functions in endocytic trafficking.PLoS genetics · 2026Article
- Integrating endogenous TurboID and data-independent acquisition mass spectrometry for in vivo proximity labeling.The EMBO journal · 2026Article
- PIKI-1, a class II phosphatidylinositol 3-kinase, functions in endocytic trafficking.bioRxiv : the preprint server for biology · 2025Article
- TAT-1, a phosphatidylserine flippase, affects molting and regulates membrane trafficking in the epidermis of Caenorhabditis elegans.Genetics · 2025Article
- Loss of the Na+/K+ cation pump CATP-1 suppresses nekl-associated molting defects.G3 (Bethesda, Md.) · 2024Article
- Dimerization activates the Inversin complex inMolecular biology of the cell · 2024Article
- Stepwise assembly of the AP2 endocytic clathrin adaptor complex.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Caenorhabditis elegans cuticle and precuticle: a model for studying dynamic apical extracellular matrices in vivo.Genetics · 2024Review
- A conserved protein tyrosine phosphatase, PTPN-22, functions in diverse developmental processes in C. elegans.PLoS genetics · 2024Article
- A conserved protein tyrosine phosphatase, PTPN-22, functions in diverse developmental processes inbioRxiv : the preprint server for biology · 2024Article
- An RNAi screen for conserved kinases that enhance microRNA activity after dauer in Caenorhabditis elegans.G3 (Bethesda, Md.) · 2024Article
- The proprotein convertase BLI-4 promotes collagen secretion prior to assembly of the Caenorhabditis elegans cuticle.PLoS genetics · 2023Article
- The proprotein convertase BLI-4 promotes collagen secretion during assembly of thebioRxiv : the preprint server for biology · 2023Article
- Conserved NIMA kinases regulate multiple steps of endocytic trafficking.PLoS genetics · 2023Article
- A spontaneousmicroPublication biology · 2023Article
- The Caenorhabditis elegans ASPP homolog APE-1 is a junctional protein phosphatase 1 modulator.Genetics · 2022Article
- An unexpected role for the conserved ADAM-family metalloprotease ADM-2 in Caenorhabditis elegans molting.PLoS genetics · 2022Article
- FCHO controls AP2's initiating role in endocytosis through a PtdIns(4,5)PScience advances · 2022Article
- A life cycle alteration can correct molting defects in Caenorhabditis elegans.Developmental biology · 2022Article
- Comprehensive Prognostic Analysis of Immune Implication Value and Oxidative Stress Significance of NECAP2 in Low-Grade Glioma.Oxidative medicine and cellular longevity · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Endocytosis, the process by which cells internalize plasma membrane and associated cargo, is regulated extensively by posttranslational modifications. Previous studies suggested the potential involvement of scores of protein kinases in endocytic control, of which only a few have been validated in vivo. Here we show that the conserved NIMA-related kinases NEKL-2/NEK8/9 and NEKL-3/NEK6/7 (the NEKLs) control clathrin-mediated endocytosis in C. elegans. Loss of NEKL-2 or NEKL-3 activities leads to penetrant larval molting defects and to the abnormal localization of trafficking markers in arrested larvae. Using an auxin-based degron system, we also find that depletion of NEKLs in adult-stage C. elegans leads to gross clathrin mislocalization and to a dramatic reduction in clathrin mobility at the apical membrane. Using a non-biased genetic screen to identify suppressors of nekl molting defects, we identified several components and regulators of AP2, the major clathrin adapter complex acting at the plasma membrane. Strikingly, reduced AP2 activity rescues both nekl mutant molting defects as well as associated trafficking phenotypes, whereas increased levels of active AP2 exacerbate nekl defects. Moreover, in a unique example of mutual suppression, NEKL inhibition alleviates defects associated with reduced AP2 activity, attesting to the tight link between NEKL and AP2 functions. We also show that NEKLs are required for the clustering and internalization of membrane cargo required for molting. Notably, we find that human NEKs can rescue molting and trafficking defects in nekl mutant worms, suggesting that the control of intracellular trafficking is an evolutionarily conserved function of NEK family kinases.
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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.