Evidence map›Paper›PMID 30955935›Full record

ArticleCurrent biology : CB2019

A CCRK and a MAK Kinase Modulate Cilia Branching and Length via Regulation of Axonemal Microtubule Dynamics in Caenorhabditis elegans.

Ashish Kumar Maurya, Travis Rogers, Piali Sengupta

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.7field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 47 citations in OpenAlex.

  1. Functions and trafficking mechanisms of RIC-8 inMolecular biology of the cell · 2026
    Article
  2. Article
  3. Joubert syndrome 26 protein enforces compartmentalized motility of a ciliary kinesin.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. The intraflagellar transport cycle.Nature reviews. Molecular cell biology · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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 · 2023
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Ashish Kumar MauryaDepartment of Biology, Brandeis University, 415 South Street, Waltham, MA 02454, USA. Electronic address: ashishkm@brandeis.edu.
Travis RogersDepartment of Biology, Brandeis University, 415 South Street, Waltham, MA 02454, USA.
Piali SenguptaDepartment of Biology, Brandeis University, 415 South Street, Waltham, MA 02454, USA. Electronic address: sengupta@brandeis.edu.
Brandeis University · US

Funding

Mechanisms of sensory neuron morphological diversification, signaling, and functional plasticityR35GM122463 · NIGMS · BRANDEIS UNIVERSITY · PI Piali Sengupta · 2017 to 2026
$7.7M
GENETIC AND BIOCHEMICAL MECHANISMS OF REGULATIONT32GM007122 · NIGMS · BRANDEIS UNIVERSITY · PI LOVETT, SUSAN THOMAS · 1985 to 2020
$7.5M
NIGMS NIH HHS R35 GM122463NIGMS NIH HHS T32 GM007122
6 · The paper itself

Abstract

The diverse morphologies of primary cilia are tightly regulated as a function of cell type and cellular state. CCRK- and MAK-related kinases have been implicated in ciliary length control in multiple species, although the underlying mechanisms are not fully understood. Here, we show that in C. elegans, DYF-18/CCRK and DYF-5/MAK act in a cascade to generate the highly arborized cilia morphologies of the AWA olfactory neurons. Loss of kinase function results in dramatically elongated AWA cilia that lack branches. Intraflagellar transport (IFT) motor protein localization, but not velocities, in AWA cilia is altered upon loss of dyf-18. We instead find that axonemal microtubules are decorated by the EBP-2 end-binding protein along their lengths and that the tubulin load is increased and tubulin turnover is reduced in AWA cilia of dyf-18 mutants. Moreover, we show that predicted microtubule-destabilizing mutations in two tubulin subunits, as well as mutations in IFT proteins predicted to disrupt tubulin transport, restore cilia branching and suppress AWA cilia elongation in dyf-18 mutants. Loss of dyf-18 is also sufficient to elongate the truncated rod-like unbranched cilia of the ASH nociceptive neurons in animals carrying a microtubule-destabilizing mutation in a tubulin subunit. We suggest that CCRK and MAK activity tunes cilia length and shape in part via modulation of axonemal microtubule stability, suggesting that similar mechanisms may underlie their roles in ciliary length control in other cell types.

Indexed as

AnimalsAxonemeCaenorhabditis elegansCaenorhabditis elegans ProteinsCiliaMicrotubulesMitogen-Activated Protein KinasesOlfactory NerveProtein Serine-Threonine KinasesCaenorhabditis elegans ProteinsDYF-18 protein, C elegansDYF-5 protein, C elegansMitogen-Activated Protein KinasesProtein Serine-Threonine KinasesAWACCRKC. elegansciliaDYF-18DYF-5IFTMAKmicrotubules

Identifiers

PMID30955935
PMCPMC6482063
OpenAlexW2933232319

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.