Evidence map›Paper›PMID 17257055›Full record

ArticlePLoS genetics2007

Gene Duplication of the zebrafish kit ligand and partitioning of melanocyte development functions to kit ligand a.

Keith A Hultman, Nathan Bahary, Leonard I Zon, Stephen L Johnson

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 13% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.

  1. Pooled it
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  7. Spotting the band.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  8. Article
  9. Article
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  11. Article
  12. Article
  13. c-Kit Receptor Maintains Sensory Axon Innervation of the Skin through Src Family Kinases.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Identification ofG3 (Bethesda, Md.) · 2020
    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

4 authors at 3 institutions in 1 country.

Keith A HultmanDepartment of Genetics, Washington University School of Medicine, Saint Louis, Missouri, United States of America.
Nathan Bahary
Leonard I Zon
Stephen L Johnson
Washington University in St. Louis · USHoward Hughes Medical Institute · USUniversity of Pittsburgh · US

Funding

REGULATION OF ADULT STEM CELLS IN ZEBRAFISHR01GM056988 · NIGMS · WASHINGTON UNIVERSITY · PI JOHNSON, STEPHEN L · 1998 to 2016
$6.0M
Genetics of latent zebrafish melanoblastsR56GM056988 · NIGMS · WASHINGTON UNIVERSITY · PI JOHNSON, STEPHEN L · 2007 to 2007
$406k
NIGMS NIH HHS GM56988NIGMS NIH HHS R01 GM056988NIGMS NIH HHS R56 GM056988
6 · The paper itself

Abstract

The retention of particular genes after the whole genome duplication in zebrafish has given insights into how genes may evolve through partitioning of ancestral functions. We examine the partitioning of expression patterns and functions of two zebrafish kit ligands, kit ligand a (kitla) and kit ligand b (kitlb), and discuss their possible coevolution with the duplicated zebrafish kit receptors (kita and kitb). In situ hybridizations show that kitla mRNA is expressed in the trunk adjacent to the notochord in the middle of each somite during stages of melanocyte migration and later expressed in the skin, when the receptor is required for melanocyte survival. kitla is also expressed in other regions complementary to kita receptor expression, including the pineal gland, tail bud, and ear. In contrast, kitlb mRNA is expressed in brain ventricles, ear, and cardinal vein plexus, in regions generally not complementary to either zebrafish kit receptor ortholog. However, like kitla, kitlb is expressed in the skin during stages consistent with melanocyte survival. Thus, it appears that kita and kitla have maintained congruent expression patterns, while kitb and kitlb have evolved divergent expression patterns. We demonstrate the interaction of kita and kitla by morpholino knockdown analysis. kitla morphants, but not kitlb morphants, phenocopy the null allele of kita, with defects for both melanocyte migration and survival. Furthermore, kitla morpholino, but not kitlb morpholino, interacts genetically with a sensitized allele of kita, confirming that kitla is the functional ligand to kita. Last, we examine kitla overexpression in embryos, which results in hyperpigmentation caused by an increase in the number and size of melanocytes. This hyperpigmentation is dependent on kita function. We conclude that following genome duplication, kita and kitla have maintained their receptor-ligand relationship, coevolved complementary expression patterns, and that functional analysis reveals that most or all of the kita receptor's function in the embryo are promoted by its interaction with kitla.

Indexed as

Gene DuplicationAnimalsBase SequenceDNA PrimersEvolution, MolecularHyperpigmentationMelanocytesMolecular Sequence DataPhylogenyRNA, MessengerStem Cell FactorZebrafishDNA PrimersRNA, MessengerStem Cell Factor

Identifiers

PMID17257055
PMCPMC1781495
OpenAlexW2019033622

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.