» Articles » PMID: 34334238

Advancing Human Disease Research with Fish Evolutionary Mutant Models

Overview
Journal Trends Genet
Specialty Genetics
Date 2021 Aug 2
PMID 34334238
Citations 13
Authors
Affiliations
Soon will be listed here.
Abstract

Model organism research is essential to understand disease mechanisms. However, laboratory-induced genetic models can lack genetic variation and often fail to mimic the spectrum of disease severity. Evolutionary mutant models (EMMs) are species with evolved phenotypes that mimic human disease. EMMs complement traditional laboratory models by providing unique avenues to study gene-by-environment interactions, modular mutations in noncoding regions, and their evolved compensations. EMMs have improved our understanding of complex diseases, including cancer, diabetes, and aging, and illuminated mechanisms in many organs. Rapid advancements of sequencing and genome-editing technologies have catapulted the utility of EMMs, particularly in fish. Fish are the most diverse group of vertebrates, exhibiting a kaleidoscope of specialized phenotypes, many that would be pathogenic in humans but are adaptive in the species' specialized habitat. Importantly, evolved compensations can suggest avenues for novel disease therapies. This review summarizes current research using fish EMMs to advance our understanding of human disease.

Citing Articles

Cichlid fishes are promising underutilized models to investigate helminth-host-microbiome interactions.

Vanhove M, Koblmuller S, Fernandes J, Hahn C, Plusquin M, Kmentova N Front Immunol. 2025; 16:1527184.

PMID: 40018030 PMC: 11864961. DOI: 10.3389/fimmu.2025.1527184.


Phylogenomic analyses of all species of swordtail fishes (genus Xiphophorus) show that hybridization preceded speciation.

Du K, Ricci J, Lu Y, Garcia-Olazabal M, Walter R, Warren W Nat Commun. 2024; 15(1):6609.

PMID: 39098897 PMC: 11298535. DOI: 10.1038/s41467-024-50852-6.


Transposable Element Expression Profiles in Premalignant Pigment Cell Lesions and Melanoma of Xiphophorus.

Munch L, Helmprobst F, Volff J, Chalopin D, Schartl M, Kneitz S Genes (Basel). 2024; 15(5).

PMID: 38790249 PMC: 11121471. DOI: 10.3390/genes15050620.


High-throughput and genome-scale targeted mutagenesis using CRISPR in a nonmodel multicellular organism, .

Ma S, Zhang T, Wang R, Wang P, Liu Y, Chang J Genome Res. 2024; 34(1):134-144.

PMID: 38191205 PMC: 10903940. DOI: 10.1101/gr.278297.123.


Cold-Driven Hemoglobin Evolution in Antarctic Notothenioid Fishes Prior to Hemoglobin Gene Loss in White-Blooded Icefishes.

Desvignes T, Bista I, Herrera K, Landes A, Postlethwait J Mol Biol Evol. 2023; 40(11).

PMID: 37879119 PMC: 10651078. DOI: 10.1093/molbev/msad236.


References
1.
Ballew B, Yeager M, Jacobs K, Giri N, Boland J, Burdett L . Germline mutations of regulator of telomere elongation helicase 1, RTEL1, in Dyskeratosis congenita. Hum Genet. 2013; 132(4):473-80. PMC: 3600110. DOI: 10.1007/s00439-013-1265-8. View

2.
Ceccaldi R, Sarangi P, DAndrea A . The Fanconi anaemia pathway: new players and new functions. Nat Rev Mol Cell Biol. 2016; 17(6):337-49. DOI: 10.1038/nrm.2016.48. View

3.
Hunter M, Moncada R, Weiss J, Yanai I, White R . Spatially resolved transcriptomics reveals the architecture of the tumor-microenvironment interface. Nat Commun. 2021; 12(1):6278. PMC: 8560802. DOI: 10.1038/s41467-021-26614-z. View

4.
Pereira M, Almeida L, Martins M, Campos M, Fraga M, Vitral R . Multiple hyperdontia: Report of an unusual case. Am J Orthod Dentofacial Orthop. 2011; 140(4):580-4. DOI: 10.1016/j.ajodo.2010.02.038. View

5.
Daane J, Rohner N, Konstantinidis P, Djuranovic S, Harris M . Parallelism and Epistasis in Skeletal Evolution Identified through Use of Phylogenomic Mapping Strategies. Mol Biol Evol. 2015; 33(1):162-73. PMC: 5009992. DOI: 10.1093/molbev/msv208. View