Evidence map›Paper›PMID 9166402›Full record

ArticleThe Journal of cell biology1997

Insertional mutation of the Drosophila nuclear lamin Dm0 gene results in defective nuclear envelopes, clustering of nuclear pore complexes, and accumulation of annulate lamellae.

B Lenz-Böhme, J Wismar, S Fuchs, R Reifegerste, E Buchner, H Betz, B Schmitt

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
4.4field-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

91 citing papers in PubMed, 230 citations in OpenAlex.

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  20. Nuclear Membrane Rupture and Its Consequences.Annual review of cell and developmental biology · 2020
    Review

31 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

B Lenz-BöhmeMax-Planck-Institut für Hirnforschung, Abteilung Neurochemie, D-60528 Frankfurt am Main, Germany.
J Wismar
S Fuchs
R Reifegerste
E Buchner
H Betz
B Schmitt
Max Planck Institute for Brain Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear lamins are thought to play an important role in disassembly and reassembly of the nucleus during mitosis. Here, we describe a Drosophila lamin Dm0 mutant resulting from a P element insertion into the first intron of the Dm0 gene. Homozygous mutant animals showed a severe phenotype including retardation in development, reduced viability, sterility, and impaired locomotion. Immunocytochemical and ultrastructural analysis revealed that reduced lamin Dm0 expression caused an enrichment of nuclear pore complexes in cytoplasmic annulate lamellae and in nuclear envelope clusters. In several cells, particularly the densely packed somata of the central nervous system, defective nuclear envelopes were observed in addition. All aspects of the mutant phenotype were rescued upon P element-mediated germline transformation with a lamin Dm0 transgene. These data constitute the first genetic proof that lamins are essential for the structural organization of the cell nucleus.

Indexed as

Drosophila ProteinsAnimalsBase SequenceBrain ChemistryCytoplasmDrosophilaEmbryo, NonmammalianFertilityFluorescent Antibody Technique, IndirectGene Expression Regulation, DevelopmentalGenes, InsectGerm-Line MutationHomozygoteIntronsLaminsLocomotionDrosophila ProteinsLaminsLam protein, DrosophilaNuclear Proteins

Identifiers

PMID9166402
PMCPMC2136230
OpenAlexW2114526838

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.