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An insight on the impact of teleost whole genome duplication on the regulation of the molecular networks controlling skeletal muscle growth
- Source :
- Scopus, Repositório Institucional da UNESP, Universidade Estadual Paulista (UNESP), instacron:UNESP, PLoS ONE, PLoS ONE, Vol 16, Iss 7, p e0255006 (2021)
- Publication Year :
- 2021
- Publisher :
- Public Library of Science (PLoS), 2021.
-
Abstract
- Made available in DSpace on 2022-05-01T06:31:27Z (GMT). No. of bitstreams: 0 Previous issue date: 2021-07-01 Fish muscle growth is a complex process regulated by multiple pathways, resulting on the net accumulation of proteins and the activation of myogenic progenitor cells. Around 350–320 million years ago, teleost fish went through a specific whole genome duplication (WGD) that expanded the existent gene repertoire. Duplicated genes can be retained by different molecular mechanisms such as subfunctionalization, neofunctionalization or redundancy, each one with different functional implications. While the great majority of ohnolog genes have been identified in the teleost genomes, the effect of gene duplication in the fish physiology is still not well characterized. In the present study we studied the effect of WGD on the transcription of the duplicated components controlling muscle growth. We compared the expression of lineage-specific ohnologs related to myogenesis and protein balance in the fast-skeletal muscle of pacus (Piaractus mesopotamicus—Ostariophysi) and Nile tilapias (Oreochromis niloticus—Acanthopterygii) fasted for 4 days and refed for 3 days. We studied the expression of 20 ohnologs and found that in the great majority of cases, duplicated genes had similar expression profiles in response to fasting and refeeding, indicating that their functions during growth have been conserved during the period after the WGD. Our results suggest that redundancy might play a more important role in the retention of ohnologs of regulatory pathways than initially thought. Also, comparison to non-duplicated orthologs showed that it might not be uncommon for the duplicated genes to gain or loss new regulatory elements simultaneously. Overall, several of duplicated ohnologs have similar transcription profiles in response to pro-growth signals suggesting that evolution tends to conserve ohnolog regulation during muscle development and that in the majority of ohnologs related to muscle growth their functions might be very similar. Department of Histology Embryology and Cell Biology Institute of Biological Sciences Federal University of Goiás (UFG), Goiás Department of Structural and Functional Biology Institute of Biosciences São Paulo State University (UNESP), Botucatu Department of Cell Biology Physiology and Immunology Faculty of Biology University of Barcelona University of Western São Paulo (UNOESTE), Presidente Prudente Fisheries Institute (IP-APTA) Department of Structural and Functional Biology Institute of Biosciences São Paulo State University (UNESP), Botucatu
- Subjects :
- Physiology
Peptide Hormones
Gene Expression
Muscle Proteins
Protein Synthesis
Muscle Development
Biochemistry
Genome
Endocrinology
0302 clinical medicine
Gene Duplication
Gene duplication
Medicine and Health Sciences
Musculoskeletal System
Phylogeny
Regulation of gene expression
0303 health sciences
Multidisciplinary
Myogenesis
Muscles
Fishes
Chemical Synthesis
Genomics
Medicine
Neofunctionalization
Anatomy
Research Article
Biosynthetic Techniques
Science
Biology
Genome Complexity
Research and Analysis Methods
Evolution, Molecular
03 medical and health sciences
Insulin-like Growth Factors
Growth Factors
DNA-binding proteins
Genetics
Animals
Gene Regulation
Muscle, Skeletal
Transcription factor
Gene
030304 developmental biology
Endocrine Physiology
Biology and Life Sciences
Proteins
Computational Biology
Duplicated Genes
Hormones
Regulatory Proteins
Skeletal Muscles
Evolutionary biology
Subfunctionalization
030217 neurology & neurosurgery
Transcription Factors
Subjects
Details
- ISSN :
- 19326203
- Volume :
- 16
- Database :
- OpenAIRE
- Journal :
- PLOS ONE
- Accession number :
- edsair.doi.dedup.....96817abd46a622995dc7ab6a98a68fe7