Evidence map›Paper›PMID 30452700›Full record

ArticleThe Journal of heredity2019

Hybrid Sterility with Meiotic Metaphase Arrest in Intersubspecific Mouse Crosses.

Risako Nishino, Sabrina Petri, Mary Ann Handel, Tetsuo Kunieda, Yasuhiro Fujiwara

Abstract read
In one paragraph

Article in The Journal of heredity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 35% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
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

5 authors at 2 institutions in 2 countries.

Risako NishinoGraduate School of Natural Science and Technology, Okayama University, Kita-ku, Okayama, Okayama, Japan.
Sabrina PetriThe Jackson Laboratory, Bar Harbor, ME, Japan.
Mary Ann HandelThe Jackson Laboratory, Bar Harbor, ME, Japan.
Tetsuo KuniedaGraduate School of Environmental and Life Science, Okayama University, Kita-ku, Okayama, Okayama, Japan.
Yasuhiro FujiwaraGraduate School of Natural Science and Technology, Okayama University, Kita-ku, Okayama, Okayama, Japan.
Okayama University · JPJackson Laboratory · US

Funding

PRDM9 and Meiotic Regulatory NetworksP01GM099640 · NIGMS · JACKSON LABORATORY · PI PAIGEN, KENNETH · 2013 to 2017
$8.2M
NIGMS NIH HHS P01 GM099640
6 · The paper itself

Abstract

Although organisms belonging to different species and subspecies sometimes produce fertile offspring, a hallmark of the speciation process is reproductive isolation, characterized by hybrid sterility (HS) due to failure in gametogenesis. In mammals, HS is usually exhibited by males, the heterogametic sex. The phenotypic manifestations of HS are complex. The most frequently observed are abnormalities in both autosomal and sex chromosome interactions that are linked to meiotic prophase arrest or postmeiotic spermiogenesis aberrations and lead to defective or absent gametes. The aim of this study was to determine the HS phenotypes in intersubspecific F1 mice produced by matings between Mus musculus molossinus-derived strains and diverse Mus musculus domesticus-inbred laboratory mouse strains. Most of these crosses produced fertile F1 offspring. However, when female BALB/cJ (domesticus) mice were mated to male JF1/MsJ (molossinus) mice, the (BALBdomxJF1mol)F1 males were sterile, whereas the (JF1molxBALBdom)F1 males produced by the reciprocal crossings were fertile; thus the sterility phenotype was asymmetric. The sterile (BALBdomxJF1mol) F1 males exhibited a high rate of meiotic metaphase arrest with misaligned chromosomes, probably related to a high frequency of XY dissociation. Intriguingly, in the sterile (BALBdomxJF1mol)F1 males we observed aberrant allele-specific expression of several meiotic genes, that play critical roles in important meiotic events including chromosome pairing. Together, these observations of an asymmetrical HS phenotype in intersubspecific F1 males, probably owing to meiotic defects in the meiotic behavior of the XY chromosomes pair and possibly also transcriptional misregulation of meiotic genes, provide new models and directions for understanding speciation mechanisms in mammals.

Indexed as

Crosses, GeneticHybridization, GeneticAllelesAnimalsApoptosisCell Cycle CheckpointsComputational BiologyFemaleGenomeGenomicsGerm CellsInfertilityMaleMeiosisMetaphaseMicehybrid sterilitymeiosismetaphaseSpo11

Identifiers

PMID30452700
PMCPMC6399516
OpenAlexW2901113416

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.