Evidence map›Paper›PMID 36098804›Full record

ArticleCellular and molecular life sciences : CMLS2022

A dominant negative mutation uncovers cooperative control of caudal Wolffian duct development by Sprouty genes.

Gisela Altés, Marta Vaquero, Sara Cuesta, Carlos Anerillas, Anna Macià, Carme Espinet, Joan Ribera, Saverio Bellusci, Ophir D Klein, Andree Yeramian and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

4 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. 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

13 authors at 3 institutions in 3 countries.

Gisela Altés *Department of Experimental Medicine, Universitat de Lleida/Institut de Recerca Biomèdica de Lleida, Edifici Biomedicina I, Lab 2.8, Rovira Roure, 80, 25198, Lleida, Spain.
Marta Vaquero *Department of Experimental Medicine, Universitat de Lleida/Institut de Recerca Biomèdica de Lleida, Edifici Biomedicina I, Lab 2.8, Rovira Roure, 80, 25198, Lleida, Spain.
Sara CuestaDepartment of Experimental Medicine, Universitat de Lleida/Institut de Recerca Biomèdica de Lleida, Edifici Biomedicina I, Lab 2.8, Rovira Roure, 80, 25198, Lleida, Spain.
Carlos AnerillasDepartment of Experimental Medicine, Universitat de Lleida/Institut de Recerca Biomèdica de Lleida, Edifici Biomedicina I, Lab 2.8, Rovira Roure, 80, 25198, Lleida, Spain.
Anna MaciàDepartment of Experimental Medicine, Universitat de Lleida/Institut de Recerca Biomèdica de Lleida, Edifici Biomedicina I, Lab 2.8, Rovira Roure, 80, 25198, Lleida, Spain.
Carme EspinetDepartment of Basic Medical Sciences, Universitat de Lleida/Institut de Recerca Biomèdica de Lleida, Rovira Roure, 80, 25198, Lleida, Spain.
Joan RiberaDepartment of Experimental Medicine, Universitat de Lleida/Institut de Recerca Biomèdica de Lleida, Edifici Biomedicina I, Lab 2.8, Rovira Roure, 80, 25198, Lleida, Spain.
Saverio BellusciJustus-Liebig University Giessen, 35392, Giessen, Germany.
Ophir D KleinDepartment of Orofacial Sciences, University of California, San Francisco, USA.
Andree YeramianDepartment of Experimental Medicine, Universitat de Lleida/Institut de Recerca Biomèdica de Lleida, Edifici Biomedicina I, Lab 2.8, Rovira Roure, 80, 25198, Lleida, Spain.
Xavi DolcetDepartment of Basic Medical Sciences, Universitat de Lleida/Institut de Recerca Biomèdica de Lleida, Rovira Roure, 80, 25198, Lleida, Spain.
Joaquim EgeaDepartment of Basic Medical Sciences, Universitat de Lleida/Institut de Recerca Biomèdica de Lleida, Rovira Roure, 80, 25198, Lleida, Spain.
Mario EncinasDepartment of Experimental Medicine, Universitat de Lleida/Institut de Recerca Biomèdica de Lleida, Edifici Biomedicina I, Lab 2.8, Rovira Roure, 80, 25198, Lleida, Spain. mario.encinas@mex.udl.cat.ORCID http://orcid.org/0000-0003-3509-7431
Universitat de Lleida · ESJustus-Liebig-Universität Gießen · DEUniversity of California, San Francisco · US

Funding

Ministerio de Ciencia, Innovación y Universidades PID2020- 114947GB-I00Ministerio de Economía y Competitividad BFU2017-83646-P
6 · The paper itself

Abstract

The Wolffian ducts (WD) are paired epithelial tubules central to the development of the mammalian genitourinary tract. Outgrowths from the WD known as the ureteric buds (UB) generate the collecting ducts of the kidney. Later during development, the caudal portion of the WD will form the vas deferens, epididymis and seminal vesicle in males, and will degenerate in females. While the genetic pathways controlling the development of the UB are firmly established, less is known about those governing development of WD portions caudal to the UB. Sprouty proteins are inhibitors of receptor tyrosine kinase (RTK) signaling in vivo. We have recently shown that homozygous mutation of a conserved tyrosine (Tyr53) of Spry1 results in UB defects indistinguishable from that of Spry1 null mice. Here, we show that heterozygosity for the Spry1 Y53A allele causes caudal WD developmental defects consisting of ectopically branched seminal vesicles in males and persistent WD in females, without affecting kidney development. Detailed analysis reveals that this phenotype also occurs in Spry1

Indexed as

OrganogenesisWolffian DuctsAnimalsFemaleMaleMammalsMiceMice, KnockoutMutationSignal TransductionTyrosineTyrosineDominant negativeGartner cystGenitourinary developmentSeminal vesicleWolffian duct

Identifiers

PMID36098804
PMCPMC9470706
OpenAlexW4295434394

What Socratic 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 Socratic graph.