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Loss of Fmr1 reorganizes the multi-elemental composition across tissues in Fragile X Syndrome mice.

Overview

Authors: Sabiha Alam1, Jamie T Reeves1, Shawn M Wilder1, Elizabeth A McCullagh1
ORCID iDs: Jamie T Reeves, Shawn M Wilder, Elizabeth A McCullagh
  1. Department of Biology, Oklahoma State University, Stillwater, Oklahoma, United States of America
Institutions: Oklahoma State University (United States)
Journal: PloS one, volume 21, issue 7, article e0352693
Dates: received 27 March 2026; accepted 13 June 2026; published online 10 July 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.1371/journal.pone.0352693 · PMID 42430454 · PMCID PMC13354080 · OpenAlex W7167932837
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: genetics / omics (modality), mouse (organism), other condition (population), cellular / molecular (subfield)
MeSH: Fragile X Messenger Ribonucleoprotein 1*, Fragile X Syndrome*, Animals, Brain, Feces, Genotype, Male, Mice, Mice, Knockout, Potassium (* major topic)
Topic: Genetics and Neurodevelopmental Disorders (Genetics, Biochemistry, Genetics and Molecular Biology), according to OpenAlex
Funding: NIGMS NIH HHS (P20 GM152333)
Citations: not cited yet (Europe PMC); 52 references in the paper

Abstract

Fragile X Syndrome (FXS) results from a genetic mutation which silences the expression of Fragile X Messenger Ribonucleoprotein (FMRP). FMRP serves various roles regulating cellular protein synthesis including mRNAs that code for proteins regulating ion flux. However, there are few studies measuring the elemental balance between FXS genotypes and tissues. Here, we measured the multivariate balance of 10 elements in tissues of wild-type and Fmr1-knockout mice to compare elemental composition of brain and somatic tissues within and across genotypes. Using a Bayesian mixed model approach, we found that the main differences between groups were between tissues, with significant effects of genotype and interaction of tissue on genotype. Wild-type feces were significantly higher in magnesium and sodium than knockout. Fur was significantly higher in potassium in wild-type, which was supported by the interaction effect of genotype with tissue. These results align with previous work showing FXS pathologies alter electrolytic and metal ion regulation, neuronal excitability, and gastrointestinal function. Future work should additionally test how elemental differences relate to function at the cellular level, as well as patterns of individual intake, digestion, assimilation, and/or excretion.

Reproduced under the paper's license (CC BY), from the paper cited above.

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Data

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Data Availability

All relevant data are within the manuscript and its Supporting information files as well as linked external data support (Figshare https://doi.org/10.6084/m9.figshare.32592354).

Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

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Version 1, 27 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 4 authors, 10 MeSH terms, 1 funder, 51 references.

Cite

This paper

Alam, S., Reeves, J. T., Wilder, S. M., & McCullagh, E. A. (2026). Loss of Fmr1 reorganizes the multi-elemental composition across tissues in Fragile X Syndrome mice. PloS one, 21(7), e0352693. https://doi.org/10.1371/journal.pone.0352693

BibTeX

@article{alam2026loss,
author = {Alam, Sabiha and Reeves, Jamie T and Wilder, Shawn M and McCullagh, Elizabeth A},
title = {{Loss of Fmr1 reorganizes the multi-elemental composition across tissues in Fragile X Syndrome mice}},
journal = {PloS one},
year = {2026},
month = jul,
volume = {21},
number = {7},
pages = {e0352693},
publisher = {PLOS},
issn = {1932-6203},
doi = {10.1371/journal.pone.0352693},
url = {https://doi.org/10.1371/journal.pone.0352693},
pmid = {42430454},
pmcid = {PMC13354080}
}

RIS

TY - JOUR
AU - Alam, Sabiha
AU - Reeves, Jamie T
AU - Wilder, Shawn M
AU - McCullagh, Elizabeth A
TI - Loss of Fmr1 reorganizes the multi-elemental composition across tissues in Fragile X Syndrome mice
T2 - PloS one
J2 - PLoS One
PY - 2026
DA - 2026/07/10
VL - 21
IS - 7
SP - e0352693
SN - 1932-6203
PB - PLOS
DO - 10.1371/journal.pone.0352693
UR - https://doi.org/10.1371/journal.pone.0352693
LA - en
ER -

CSL-JSON

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