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Journal Article

Exploring the Fanconi Anemia Gene Expression and Regulation by MicroRNAs in Gilthead Seabream (Sparus aurata) at Different Gonadal Development Stages

Maria Papadaki; Ngoc-Son Le; Constantinos C. Mylonas; Elena Sarropoulou
Marine Biotechnology · Vol. 27, Issue 2 · 2025

Abstract

Fanconi anaemia (FA) is a rare autosomal recessive disease in humans that is distributed worldwide. Fanconi anemia complementation (Fanc) proteins are essential for the appropriate functioning of the FA DNA repair pathway. They are also linked to a number of other biological processes, including oxygen metabolism, cell cycle regulation, haematopoiesis and apoptosis. So far, little research has been conducted on teleosts, but evidence shows that Fanc proteins play a significant role in immune response and sex reversal. For the examination of the expression of three fanc genes ( fancc , fancl, and fancd2 ), as well as the potential regulation of these genes by microRNAs (miRNAs) in gonadal tissues at different stages of development, the present study has selected the gilthead seabream ( Sparus aurata ), a significant aquaculture species that exhibits protandrous hermaphroditism. The obtained data suggested the role of fancl and fancd2 in the maturation of female gonads and the miRNAs miR-210, miR-217 and miR-10926 have been identified as putative regulators of fancd2 , fancc and fancl , respectively. Overall, the data indicated the potential use of fancl and fancd2 genes as sex biomarkers in conjunction with their respective regulation by miRNAs. To the best of our knowledge, this is the first study demonstrating the importance of fanc genes, along with putative regulatory miRNAs, in the reproduction of an important marine aquaculture species.

Bibliographic Information

JournalMarine Biotechnology
PublisherSpringer
Publication Date2025-04-01
Publication Year2025
Volume27
Issue2
Document TypeJournal Article
Print ISSN1436-2228
eISSN1436-2236
DOI10.1007/s10126-025-10444-x

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NARA Access Coverage1999-01-01~Current
Journal Homepagehttps://www.springer.com/journal/10126
Publisher PageOpen Publisher Page
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