Evidence map›Paper›PMID 38299894›Full record

ArticleThe Journal of physiology2024

Genetic influences on motor learning and performance and superperforming mutants revealed by random mutational survey of the mouse genome.

Vikram Jakkamsetti, Qian Ma, Gustavo Angulo, William Scudder, Bruce Beutler, Juan M Pascual

Open access · hybridAbstract read
In one paragraph

Article in The Journal of physiology, 2024. 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
–field-weighted citation impact, top 99% 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, 0 citations in OpenAlex.

  1. CTRP10 is required for optimal motor function.The Journal of biological chemistry · 2026
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Vikram JakkamsettiRare Brain Disorders Program, Department of Neurology, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Qian MaRare Brain Disorders Program, Department of Neurology, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.ORCID 0000-0003-0788-1843
Gustavo AnguloRare Brain Disorders Program, Department of Neurology, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
William ScudderRare Brain Disorders Program, Department of Neurology, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Bruce BeutlerCenter for Genetics of Host Defense, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Juan M PascualRare Brain Disorders Program, Department of Neurology, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.ORCID 0000-0002-0843-8221
The University of Texas Southwestern Medical Center · USSouthwestern Medical Center · USCenter for Human Genetics · US

Funding

UT Southwestern NORCP30DK127984 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI Jeff G McDonald · 2022 to 2026
$7.4M
Mechanisms of Motor SuperperformanceR01NS133439 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI Juan M. Pascual · 2024 to 2026
$1.7M
Mechanisms of motor superperformanceR56NS121993 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI PASCUAL, JUAN M. · 2022 to 2022
$540k
NIDDK NIH HHS P30 DK127984NINDS NIH HHS R01 NS133439NINDS NIH HHS R56 NS121993
6 · The paper itself

Abstract

Evolution depends upon genetic variations that influence physiology. As defined in a genetic screen, phenotypic performance may be enhanced or degraded by such mutations. We set out to detect mutations that influence motor function, including motor learning. Thus, we tested the motor effects of 36,444 non-synonymous coding/splicing mutations induced in the germline of C57BL/6J mice with N-ethyl-N-nitrosourea by measuring changes in the performance of repetitive rotarod trials while blinded to genotype. Automated meiotic mapping was used to implicate individual mutations in causation. In total, 32,726 mice bearing all the variant alleles were screened. This was complemented with the simultaneous testing of 1408 normal mice for reference. In total, 16.3% of autosomal genes were thus rendered detectably hypomorphic or nullified by mutations in homozygosity and motor tested in at least three mice. This approach allowed us to identify superperformance mutations in Rif1, Tk1, Fan1 and Mn1. These genes are primarily related, among other less well-characterized functions, to nucleic acid biology. We also associated distinct motor learning patterns with groups of functionally related genes. These functional sets included, preferentially, histone H3 methyltransferase activity for mice that learnt at an accelerated rate relative to the remaining mutant mice. The results allow for an estimation of the fraction of mutations that can modify a behaviour influential for evolution such as locomotion. They may also enable, once the loci are further validated and the mechanisms elucidated, the harnessing of the activity of the newly identified genes to enhance motor ability or to counterbalance disability or disease. KEY POINTS: We studied the effect of chemically induced random mutations on mouse motor performance. An array of mutations influenced the rate of motor learning. DNA regulation genes predominated among these mutant loci. Several mutations in unsuspected genes led to superperformance. Assuming little-biased mutagenicity, the results allow for an estimation of the probability for any spontaneous mutation to influence a behaviour such as motor learning and ultimate performance.

Indexed as

Mice, Inbred C57BLMutationAnimalsFemaleGenomeLearningMaleMiceMotor ActivityCRISPRENUmotormutagenesis

Identifiers

PMID38299894
PMCPMC11142877
OpenAlexW4391449935

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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.