Evidence map›Paper›PMID 33147376›Full record

ArticleGenes to cells : devoted to molecular & cellular mechanisms2021

Periodic albinism of a widely used albino mutant of Xenopus laevis caused by deletion of two exons in the Hermansky-Pudlak syndrome type 4 gene.

Toshihiko Fukuzawa

Open access · hybridAbstract read
In one paragraph

Article in Genes to cells : devoted to molecular & cellular mechanisms, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Control Strategies in Guanine Biocrystallization.Angewandte Chemie (International ed. in English) · 2026
    Review
  2. Tyrosinase-Deficient Skin Melanophore Lineage inInternational journal of molecular sciences · 2026
    Article
  3. Review
  4. Article
  5. AlbinomicroPublication biology · 2023
    Article
  6. Article
  7. Review
  8. 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

1 author at 1 institution in 1 country.

Toshihiko FukuzawaDepartment of Biology, Keio University, Yokohama, Japan.ORCID https://orcid.org/0000-0002-8624-393X
Keio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The periodic albino mutant of Xenopus laevis is a recessive mutant, in which reduced amounts of melanin appear in the retinal pigment epithelium (RPE) and in melanophores at the late embryonic stage, after which both RPE and melanophores gradually depigment. Three types of pigment cells (melanophores, iridophores and xanthophores) have been reported to be affected in this albino. However, the causative gene of the periodic albinism remains unknown. Hermansky-Pudlak syndrome (HPS) is an autosomal recessive disorder that affects humans and mice, which is caused by defective biogenesis of lysosome-related organelles (LROs). Two subgenomes (L and S) are present in the allotetraploid frog X. laevis. Comparison of genes between the chromosomes 1L and 1S revealed that the HPS type 4 (hps4) gene was present only in chromosome 1L. In the albino mutant, a 1.9 kb genomic deletion in the hps4.L gene including exons 7 and 8 caused a premature stop codon to create a truncated Hps4 protein. Injection of wild-type hps4.L mRNA into mutant embryos rescued the albino phenotype. These findings indicate that hps4 is a causative gene for the periodic albinism in X. laevis. The phenotype of this mutant should be reassessed from the perspective of LRO biogenesis.

Indexed as

Gene DeletionAlbinismAnimalsExonsPolyploidyXenopus laevisXenopus ProteinsXenopus ProteinsalbinismHermansky-Pudlak syndromemelanophoresmutationperiodic albinoretinal pigment epitheliumXenopus laevis

Identifiers

PMID33147376
PMCPMC7839477
OpenAlexW3096475254

What OpenQuestion holds

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Registered trials

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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.