Evidence map›Paper›PMID 24963054›Full record

ArticleThe Plant cell2014

The jiaoyao1 Mutant Is an Allele of korrigan1 That Abolishes Endoglucanase Activity and Affects the Organization of Both Cellulose Microfibrils and Microtubules in Arabidopsis.

Lei Lei, Tian Zhang, Richard Strasser, Christopher M Lee, Martine Gonneau, Lukas Mach, Samantha Vernhettes, Seong H Kim, Daniel J Cosgrove, Shundai Li and 1 more

Open access · greenAbstract read
In one paragraph

Article in The Plant cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
14.5field-weighted citation impact, top 1% 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

33 citing papers in PubMed, 74 citations in OpenAlex.

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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

11 authors at 3 institutions in 3 countries.

Lei LeiDepartment of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, Pennsylvania 16802.
Tian ZhangDepartment of Biology, Pennsylvania State University, University Park, Pennsylvania 16802.
Richard StrasserDepartment of Applied Genetics and Cell Biology, University of Natural Resources and Life Sciences, A-1190 Vienna, Austria.
Christopher M LeeChemical Engineering and Materials Research Institute, Pennsylvania State University, University Park, Pennsylvania 16802.
Martine GonneauInstitut Jean-Pierre Bourgin, Unité Mixte de Recherche 1318 INRA-AgroParisTech, 78026 Versailles, France.
Lukas MachDepartment of Applied Genetics and Cell Biology, University of Natural Resources and Life Sciences, A-1190 Vienna, Austria.
Samantha VernhettesDepartment of Applied Genetics and Cell Biology, University of Natural Resources and Life Sciences, A-1190 Vienna, Austria.
Seong H KimChemical Engineering and Materials Research Institute, Pennsylvania State University, University Park, Pennsylvania 16802.
Daniel J CosgroveDepartment of Biology, Pennsylvania State University, University Park, Pennsylvania 16802.
Shundai LiDepartment of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, Pennsylvania 16802.
Ying GuDepartment of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, Pennsylvania 16802 yug13@psu.edu.
Pennsylvania State University · USAgroParisTech · FRBOKU University · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In higher plants, cellulose is synthesized by plasma membrane-localized cellulose synthase complexes (CSCs). Arabidopsis thaliana GH9A1/KORRIGAN1 is a membrane-bound, family 9 glycosyl hydrolase that is important for cellulose synthesis in both primary and secondary cell walls. Most previously identified korrigan1 mutants show severe phenotypes such as embryo lethality; therefore, the role of GH9A1 in cellulose synthesis remains unclear. Here, we report a novel A577V missense mutation, designated jiaoyao1 (jia1), in the second of the glycosyl hydrolase family 9 active site signature motifs in GH9A1. jia1 is defective in cell expansion in dark-grown hypocotyls, roots, and adult plants. Consistent with its defect in cell expansion, this mutation in GH9A1 resulted in reduced cellulose content and reduced CSC velocity at the plasma membrane. Green fluorescent protein-GH9A1 is associated with CSCs at multiple locations, including the plasma membrane, Golgi, trans-Golgi network, and small CESA-containing compartments or microtubule-associated cellulose synthase compartments, indicating a tight association between GH9A1 and CSCs. GH9A1

Identifiers

PMID24963054
PMCPMC4114954
OpenAlexW2111335508

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.