Evidence map›Paper›PMID 24627485›Full record

ArticleThe Journal of biological chemistry2014

The nuclear pore complex function of Sec13 protein is required for cell survival during retinal development.

Xubo Niu, Jian Hong, Xiaofeng Zheng, David B Melville, Ela W Knapik, Anming Meng, Jinrong Peng

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. 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
0.7field-weighted citation impact, top 30% 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, 54 citations in OpenAlex.

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  15. Review
  16. Article
  17. Nucleoporins in cardiovascular disease.Journal of molecular and cellular cardiology · 2020
    Review
  18. Article
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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 5 institutions in 2 countries.

Xubo NiuKey Laboratory for Molecular Animal Nutrition, Ministry of Education, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China.
Jian HongInstitute of Biotechnology, Zhejiang University, Hangzhou 310058, China.
Xiaofeng ZhengState Key Laboratory of Biomembrane and Membrane Engineering, Tsinghua-Peking Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing 100084, China.
David B MelvilleDepartment of Molecular and Cell Biology, University of California at Berkeley, Berkeley, California 94720-3370; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232.
Ela W KnapikDepartment of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232.
Anming MengState Key Laboratory of Biomembrane and Membrane Engineering, Tsinghua-Peking Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Jinrong PengKey Laboratory for Molecular Animal Nutrition, Ministry of Education, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China. Electronic address: pengjr@zju.edu.cn.
Zhejiang University · CNCenter for Life Sciences · CNTsinghua University · CNUniversity of California, Berkeley · USVanderbilt University Medical Center · US

Funding

TRAINING PROGRAM IN CELLULAR, BIOCHEMICAL, &MOLECULAR ST32GM008554 · NIGMS · VANDERBILT UNIVERSITY · PI PATTON, JAMES G. · 1995 to 2020
$7.4M
THE ROLE OF THE SECRETORY PATHWAY IN CRANIOFACIAL MORPHOGENESISR01DE018477 · NIDCR · VANDERBILT UNIVERSITY · PI KNAPIK, ELA W · 2007 to 2010
$1.5M
NIDCR NIH HHS R01 DE018477NIGMS NIH HHS T32 GM008554
6 · The paper itself

Abstract

Sec13 is a dual function protein, being a core component of both the COPII coat, which mediates protein trafficking from the endoplasmic reticulum to the Golgi apparatus, and the nuclear pore complex (NPC), which facilitates nucleo-cytoplasmic traffic. Here, we present a genetic model to differentiate the roles of these two functions of Sec13 in vivo. We report that sec13(sq198) mutant embryos develop small eyes that exhibit disrupted retinal lamination and that the mutant retina contains an excessive number of apoptotic cells. Surprisingly, we found that loss of COPII function by oligonucleotide-mediated gene knockdown of sec31a and sec31b or brefeldin A treatment did not disrupt retinal lamination, although it did result in digestive organ defects similar to those seen in sec13(sq198), suggesting that the digestive organ defects observed in sec13(sq198) are due to loss of COPII function, whereas the retinal lamination defects are due to loss of the NPC function. We showed that the retinal cells of sec13(sq198) failed to form proper nuclear pores, leading to a nuclear accumulation of total mRNA and abnormal activation of the p53-dependent apoptosis pathway, causing the retinal defect in sec13(sq198). Furthermore, we found that a mutant lacking Nup107, a key NPC-specific component, phenocopied the retinal lamination phenotype as observed in sec13(sq198). Our results demonstrate a requirement for the nuclear pore function of Sec13 in development of the retina and provide the first genetic evidence to differentiate the contributions of the NPC and the COPII functions of Sec13 during organogenesis.

Indexed as

AnimalsBase SequenceDNA PrimersIn Situ HybridizationMicroscopy, Electron, TransmissionNuclear PoreReal-Time Polymerase Chain ReactionRetinaRNA, MessengerZebrafishZebrafish ProteinsDNA PrimersRNA, MessengerZebrafish ProteinsCell BiologyEndoplasmic Reticulum (ER)Molecular GeneticsNuclear Pore Complexesp53Retina DevelopmentSec13Sec31Zebrafish

Identifiers

PMID24627485
PMCPMC4002104
OpenAlexW2061455429

What OpenQuestion holds

Textmetadata
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.