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mIMCD-3

RRID:CVCL_0429

Organism

Mus musculus

Comments

Transformant: NCBI_TaxID; 1891767; Simian virus 40 (SV40). Breed/subspecies: Tg(SV40E)Bri/7 transgenic. DT Created: 04-04-12; Last updated: 05-07-19; Version: 14

Proper Citation

ATCC Cat# CRL-2123, RRID:CVCL_0429

Category

Transformed cell line DT Created: 04-04-12; Last updated: 05-07-19; Version: 14

Sex

DT Created: 04-04-12; Last updated: 05-07-19; Version: 14

Synonyms

mIMCD3, IMCD-3, IMCD3, mouse Inner Medullary Collecting Duct-3 DT Created: 04-04-12, Last updated: 05-07-19, Version: 14

Vendor

ATCC

Cat Num

CRL-2123

Cross References

BTO; BTO:0003913 CLO; CLO_0007730 EFO; EFO_0002073 MCCL; MCC:0000500 ATCC; CRL-2123 BioSample; SAMN11397642 Lonza; 10 Wikidata; Q28472922 DT Created: 04-04-12; Last updated: 05-07-19; Version: 14

Hierarchy

DT Created: 04-04-12; Last updated: 05-07-19; Version: 14

Originate from Same Individual

DT Created: 04-04-12; Last updated: 05-07-19; Version: 14

Publications that use this research resource

Primary Cilia Signaling Shapes the Development of Interneuronal Connectivity.

  • Guo J
  • Dev. Cell
  • 2017 Aug 7

Literature context:


Abstract:

Appropriate growth and synaptic integration of GABAergic inhibitory interneurons are essential for functional neural circuits in the brain. Here, we demonstrate that disruption of primary cilia function following the selective loss of ciliary GTPase Arl13b in interneurons impairs interneuronal morphology and synaptic connectivity, leading to altered excitatory/inhibitory activity balance. The altered morphology and connectivity of cilia mutant interneurons and the functional deficits are rescued by either chemogenetic activation of ciliary G-protein-coupled receptor (GPCR) signaling or the selective induction of Sstr3, a ciliary GPCR, in Arl13b-deficient cilia. Our results thus define a specific requirement for primary cilia-mediated GPCR signaling in interneuronal connectivity and inhibitory circuit formation.

Funding information:
  • NIDDK NIH HHS - P30 DK074038()
  • NIMH NIH HHS - R01 MH060929()
  • NINDS NIH HHS - P30 NS045892()
  • NINDS NIH HHS - R01 NS090029()
  • NINDS NIH HHS - R56 NS090029()

IFT trains in different stages of assembly queue at the ciliary base for consecutive release into the cilium.

  • Wingfield JL
  • Elife
  • 2017 May 31

Literature context:


Abstract:

Intraflagellar transport (IFT) trains, multimegadalton assemblies of IFT proteins and motors, traffic proteins in cilia. To study how trains assemble, we employed fluorescence protein-tagged IFT proteins in Chlamydomonas reinhardtii. IFT-A and motor proteins are recruited from the cell body to the basal body pool, assembled into trains, move through the cilium, and disperse back into the cell body. In contrast to this 'open' system, IFT-B proteins from retrograde trains reenter the pool and a portion is reused directly in anterograde trains indicating a 'semi-open' system. Similar IFT systems were also observed in Tetrahymena thermophila and IMCD3 cells. FRAP analysis indicated that IFT proteins and motors of a given train are sequentially recruited to the basal bodies. IFT dynein and tubulin cargoes are loaded briefly before the trains depart. We conclude that the pool contains IFT trains in multiple stages of assembly queuing for successive release into the cilium upon completion.

Dynamic Remodeling of Membrane Composition Drives Cell Cycle through Primary Cilia Excision.

  • Phua SC
  • Cell
  • 2017 Jan 12

Literature context:


Abstract:

The life cycle of a primary cilium begins in quiescence and ends prior to mitosis. In quiescent cells, the primary cilium insulates itself from contiguous dynamic membrane processes on the cell surface to function as a stable signaling apparatus. Here, we demonstrate that basal restriction of ciliary structure dynamics is established by the cilia-enriched phosphoinositide 5-phosphatase, Inpp5e. Growth induction displaces ciliary Inpp5e and accumulates phosphatidylinositol 4,5-bisphosphate in distal cilia. This change triggers otherwise-forbidden actin polymerization in primary cilia, which excises cilia tips in a process we call cilia decapitation. While cilia disassembly is traditionally thought to occur solely through resorption, we show that an acute loss of IFT-B through cilia decapitation precedes resorption. Finally, we propose that cilia decapitation induces mitogenic signaling and constitutes a molecular link between the cilia life cycle and cell-division cycle. This newly defined ciliary mechanism may find significance in cell proliferation control during normal development and cancer.

Funding information:
  • NIAMS NIH HHS - R01 AR054396()
  • NIDDK NIH HHS - R01 DK102910()
  • NIGMS NIH HHS - DP2 GM105448()
  • NIGMS NIH HHS - R01 GM095941()
  • NIGMS NIH HHS - R01 GM112988()

Centriole distal appendages promote membrane docking, leading to cilia initiation.

  • Tanos BE
  • Genes Dev.
  • 2013 Jan 15

Literature context:


Abstract:

The distal appendages (DAPs) of centrioles have been proposed to anchor cilia to the plasma membrane, but their molecular composition, assembly, and exact function in ciliogenesis remain poorly understood. Using quantitative centrosome proteomics and superresolution microscopy, we identified five DAP components, including one previously described (CEP164), one partially characterized (CEP89 [ccdc123]), and three novel (CEP83 [ccdc41], SCLT1, and FBF1) DAP proteins. Analyses of DAP assembly revealed a hierarchy. CEP83 recruits both SCLT1 and CEP89 to centrioles. Subsequent recruitment of FBF1 and CEP164 is independent of CEP89 but mediated by SCLT1. All five DAP components are essential for ciliogenesis; loss of CEP83 specifically blocks centriole-to-membrane docking. Undocked centrioles fail to recruit TTBK2 or release CP110, the two earliest modifications found on centrioles prior to cilia assembly, revealing centriole-to-membrane docking as a temporal and spatial cue promoting cilia initiation.

Funding information:
  • NCI NIH HHS - P30 CA008748()
  • NCRR NIH HHS - S10 RR031855()
  • NCRR NIH HHS - S10RR031855()
  • NIGMS NIH HHS - F32 GM096558()
  • NIGMS NIH HHS - GM088253()
  • NIGMS NIH HHS - GM096558()
  • NIGMS NIH HHS - R01 GM088253()
  • NINDS NIH HHS - R21 NS054143(United States)