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Fishes
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Genomics Applied to Fish Health
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Genomics Applied to Fish Health

A special issue of Fishes (ISSN 2410-3888). This special issue belongs to the section "Welfare, Health and Disease".

Deadline for manuscript submissions: 20 March 2026 | Viewed by 2234

Special Issue Editor

Dr. Phillip Dettleff

E-Mail Website
Guest Editor
School of Veterinary Medicine, Pontifical Catholic University of Chile, Santiago 8320165, Chile
Interests: aquaculture; genomics; environmental stressors; host-pathogen interaction

Special Issue Information

Dear Colleagues,

The sustainability and growth of aquaculture are essential to meeting the increased demand for global food production, and high-quality protein production from aquatic animals and algae is key to supplying this demand and contributing to food security. Achieving a better understanding of the biological problems (nutrition, pathogens, reproduction, and environment) in aquaculture species is crucial to realizing sustainable aquaculture, and the impact of genomics upon fish health is relevant for the promotion of the sustainability of aquaculture or natural populations. Genomic research could provide relevant information to solve these problems, including information on gene structure and function, pathway regulation, transcriptional response, and protein changes.

This Special Issue aims to publish high-quality, novel research on all fields of genomics applied to fish health, including all fish species, whether from aquaculture or natural populations. Manuscripts on established species, as well as new species for aquaculture diversification, are welcome. This Special Issue aims to publish contributions that focus on the study of genomics, including the functional response of genes and proteins in fish (including the transcriptomics of coding or non-coding RNAs, proteomics, etc.), as well as gene editing applied to aquaculture species, in a context of fish health, including infectious or metabolic diseases or environmental effects upon health. We welcome original articles and reviews that cover any of the related topics.

Dr. Phillip Dettleff
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Fishes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • aquaculture
  • genomics
  • transcriptomics
  • proteomics
  • sustainability
  • fish health
  • infectious disease
  • metabolic diseases

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

13 pages, 1973 KB  
Article
Non-Genomic Cortisol Signaling Regulates Early Myogenic Gene Expression in Rainbow Trout Skeletal Muscle
by Consuelo Figueroa, Rodrigo Zuloaga, Giorgia Daniela Ugarte, Phillip Dettleff, Jorge Eduardo Aedo, Alfredo Molina and Juan Antonio Valdés
Fishes 2025, 10(12), 621; https://doi.org/10.3390/fishes10120621 - 4 Dec 2025
Viewed by 185
Abstract
Glucocorticoids are key regulators of vertebrate physiology, orchestrating metabolic, immune, and developmental processes that enable adaptation to stress. In teleosts, cortisol is the primary glucocorticoid, acting through classical genomic pathways and rapid non-genomic mechanisms. Although genomic signaling has been widely characterized, non-genomic actions [...] Read more.
Glucocorticoids are key regulators of vertebrate physiology, orchestrating metabolic, immune, and developmental processes that enable adaptation to stress. In teleosts, cortisol is the primary glucocorticoid, acting through classical genomic pathways and rapid non-genomic mechanisms. Although genomic signaling has been widely characterized, non-genomic actions remain poorly understood in skeletal muscle, a tissue of both biological and economic importance. In this study, we examined the effects of cortisol and its membrane-impermeable analog, cortisol-BSA, on rainbow trout (Oncorhynchus mykiss) skeletal muscle under in vivo and in vitro conditions. Transcript analysis demonstrated that cortisol and cortisol-BSA rapidly induced pax3 (2.28 ± 0.22- and 2.48 ± 0.45-fold change, respectively) and myf5 expression (3.03 ± 0.47- and 2.31 ± 0.29-fold change, respectively) at 1 h, whereas prolonged cortisol and cortisol-BSA exposure resulted in their downregulation (0.34 ± 0.07- and 0.38 ± 0.14-fold change, respectively). In cultured myotubes, cortisol-BSA activated protein kinase A (PKA) (2.24 ± 0.25-fold change) and enhanced phosphorylation of its downstream target CREB (3.2 ± 0.21-fold change) in a time-dependent manner; these effects were abolished by the PKA inhibitor H89. Moreover, inhibition of PKA signaling suppressed cortisol-BSA–induced pax3 and myf5 expression (1.31 ± 0.28-fold change and 1.89 ± 0.28-fold change, respectively). Together, these findings provide the first mechanistic evidence that non-genomic cortisol signaling regulates the PKA–CREB axis in fish skeletal muscle, promoting the early transcriptional activation of promyogenic factors. This work underscores the complementary role of rapid cortisol actions in fine-tuning myogenic responses under acute stress, offering new perspectives on muscle plasticity in teleosts. Full article
(This article belongs to the Special Issue Genomics Applied to Fish Health)
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13 pages, 5120 KB  
Article
Hepcidin Deficiency Disrupts Iron Homeostasis and Induces Ferroptosis in Zebrafish Liver
by Mingli Liu, Mingjian Peng, Jingwen Ma, Ruiqin Hu, Qianghua Xu, Peng Hu and Liangbiao Chen
Fishes 2025, 10(5), 243; https://doi.org/10.3390/fishes10050243 - 21 May 2025
Cited by 2 | Viewed by 1654
Abstract
Hepcidin is a key regulator of systemic iron homeostasis, which is essential for maintaining iron balance and cellular health. To investigate its role in zebrafish, we empolyed a hepcidin knockout model. Morphological and histological analyses revealed pale livers and significant iron accumulation in [...] Read more.
Hepcidin is a key regulator of systemic iron homeostasis, which is essential for maintaining iron balance and cellular health. To investigate its role in zebrafish, we empolyed a hepcidin knockout model. Morphological and histological analyses revealed pale livers and significant iron accumulation in hep−/− zebrafish, particularly in liver, skin, and egg tissues. RNA sequencing identified 1,424 differentially expressed genes (DEGs) between wild-type (WT) and hep−/− zebrafish, with significant enrichment in pathways related to ferroptosis, fatty acid degradation, and heme binding. Western blot analysis showed reduced levels of key iron-related proteins, including GPX4, Fth1, and ferroportin (FPN), indicating impaired iron transport and increased oxidative stress. Gene Ontology (GO) and KEGG analyses highlighted disruptions in iron metabolism and lipid oxidation, linking iron overload to ferroptosis in the absence of hepcidin. These findings demonstrate that hepcidin deficiency leads to profound dysregulation of iron homeostasis, driving lipid peroxidation and ferroptosis in the zebrafish liver. Our study provides mechanistic insights into the molecular consequences of hepcidin loss, advancing our understanding of iron-related oxidative damage and its physiological impacts. Full article
(This article belongs to the Special Issue Genomics Applied to Fish Health)
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