Evidence map›Paper›PMID 26997941›Full record

ArticleMolecular syndromology2016

Multiple Small Supernumerary Marker Chromosomes Resulting from Maternal Meiosis I or II Errors.

Ron Hochstenbach, Beata Nowakowska, Marianne Volleth, Amber Ummels, Anna Kutkowska-Kaźmierczak, Ewa Obersztyn, Kamila Ziemkiewicz, Claudia Gerloff, Denny Schanze, Martin Zenker and 4 more

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In one paragraph

Article in Molecular syndromology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

7 citing papers in PubMed, 11 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

14 authors at 3 institutions in 2 countries.

Ron HochstenbachDivision of Biomedical Genetics, Department of Medical Genetics, University Medical Center Utrecht, Utrecht, The Netherlands.
Beata NowakowskaDepartment of Medical Genetics, Institute of the Mother and Child, Warsaw, Poland.
Marianne VollethDepartment of Human Genetics, Magdeburg, Germany.
Amber UmmelsDivision of Biomedical Genetics, Department of Medical Genetics, University Medical Center Utrecht, Utrecht, The Netherlands.
Anna Kutkowska-KaźmierczakDepartment of Medical Genetics, Institute of the Mother and Child, Warsaw, Poland.
Ewa ObersztynDepartment of Medical Genetics, Institute of the Mother and Child, Warsaw, Poland.
Kamila ZiemkiewiczDepartment of Medical Genetics, Institute of the Mother and Child, Warsaw, Poland.
Claudia GerloffUniversity Women's Clinic, Otto-von-Guericke University, Magdeburg, Germany.
Denny SchanzeDepartment of Human Genetics, Magdeburg, Germany.
Martin ZenkerDepartment of Human Genetics, Magdeburg, Germany.
Petra MuschkeDepartment of Human Genetics, Magdeburg, Germany.
Ina SchanzeDepartment of Human Genetics, Magdeburg, Germany.
Martin PootDivision of Biomedical Genetics, Department of Medical Genetics, University Medical Center Utrecht, Utrecht, The Netherlands.
Thomas LiehrDepartment of Human Genetics, University Clinic, Jena, Germany.
University Medical Center Utrecht · NLJena University Hospital · DEOtto-von-Guericke University Magdeburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We present 2 cases with multiple de novo supernumerary marker chromosomes (sSMCs), each derived from a different chromosome. In a prenatal case, we found mosaicism for an sSMC(4), sSMC(6), sSMC(9), sSMC(14) and sSMC(22), while a postnatal case had an sSMC(4), sSMC(8) and an sSMC(11). SNP-marker segregation indicated that the sSMC(4) resulted from a maternal meiosis II error in the prenatal case. Segregation of short tandem repeat markers on the sSMC(8) was consistent with a maternal meiosis I error in the postnatal case. In the latter, a boy with developmental/psychomotor delay, autism, hyperactivity, speech delay, and hypotonia, the sSMC(8) was present at the highest frequency in blood. By comparison to other patients with a corresponding duplication, a minimal region of overlap for the phenotype was identified, with CHRNB3 and CHRNA6 as dosage-sensitive candidate genes. These genes encode subunits of nicotinic acetylcholine receptors (nAChRs). We propose that overproduction of these subunits leads to perturbed component stoichiometries with dominant negative effects on the function of nAChRs, as was shown by others in vitro. With the limitation that in each case only one sSMC could be studied, our findings demonstrate that different meiotic errors lead to multiple sSMCs. We relate our findings to age-related aneuploidy in female meiosis and propose that predivision sister-chromatid separation during meiosis I or II, or both, may generate multiple sSMCs.

Indexed as

CHRNA6CHRNB3Dominant negative effectMaternal meiotic segregation errorMental retardationMultiple supernumerary marker chromosomesNicotinic acetylcholine receptorsPredivision chromatid separation

Identifiers

PMID26997941
PMCPMC4772618
OpenAlexW2197578641

What OpenQuestion holds

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Read underepoch 390

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.