The cause of hybrid sterility and inviability has not been analyzed in the fin-fish hybrid, although large numbers of hybridizations have been carried out. In this study, we produced allo-diploid hybrids by cross-fertilization between female goldfish (Carassius auratus) and male golden venus chub (Hemigrammocypris rasborella). Inviability of these hybrids was due to breakage of the enveloping layer during epiboly or due to malformation with serious cardiac oedema around the hatching stage. Spontaneous allo-triploid hybrids with two sets of the goldfish genome and one set of the golden venus chub genome developed normally and survived beyond the feeding stage. This improved survival was confirmed by generating heat-shock-induced allo-triploid hybrids that possessed an extra goldfish genome. When inviable allo-diploid hybrid cells were transplanted into goldfish host embryos at the blastula stage, these embryos hatched normally, incorporating the allo-diploid cells. These allo-diploid hybrid cells persisted, and were genetically detected in a 6-month-old fish. In contrast, primordial germ cells taken from allo-diploid hybrids and transplanted into goldfish hosts at the blastula stage had disappeared by 10 days post-fertilization, even under chimeric conditions. In allo-triploid hybrid embryos, germ cells proliferated in the gonad, but had disappeared by 10 weeks post-fertilization. These results showed that while hybrid germ cells are inviable even in chimeric conditions, hybrid somatic cells remain viable.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1017/S0967199420000349 | DOI Listing |
Commun Biol
January 2025
Université Paris Cité, CNRS, Inserm, Institut Cochin, F-75014, Paris, France.
The H3K79 methyltransferase DOT1L is essential for multiple aspects of mammalian development where it has been shown to regulate gene expression. Here, by producing and integrating epigenomic and spike-in RNA-seq data, we decipher the molecular role of DOT1L during mouse spermatogenesis and show that it has opposite effects on gene expression depending on chromatin environment. On one hand, DOT1L represses autosomal genes that are devoid of H3K79me2 at their bodies and located in H3K27me3-rich/H3K27ac-poor environments.
View Article and Find Full Text PDFSci Rep
January 2025
Animal Genomics Laboratory, Animal Biotechnology Division, ICAR-National Dairy Research Institute, Karnal, Haryana, India.
Poor male fertility significantly affects dairy production, primarily due to low conception rates (CR) in bulls, even when cows are inseminated with morphologically normal sperm. Seminal plasma is a key factor in evaluating the fertilizing ability of bull semen. The extracellular vesicles (EVs) in seminal plasma contain fertility-associated proteins like SPAM1, ADAM7, and SP10, which influence sperm function and fertilizing potential.
View Article and Find Full Text PDFReprod Fertil Dev
January 2025
CNRS, INRAE, Université de Tours, PRC, Nouzilly, France.
Female infertility, which affects 10-20% of couples worldwide, is a growing health concern in developing countries. It can be caused by multiple factors, including reproductive disorders, hormonal dysfunctions, congenital malformations and infections. In vitro and in vivo studies have shown that plant extracts regulate gonadotropin-releasing hormone, kisspeptin, and gonadotropin expression and/or secretion at the hypothalamic-pituitary level and modulate somatic and germ cells, such as steroidogenesis, proliferation, apoptosis, and oxidative stress at the ovarian level.
View Article and Find Full Text PDFElife
January 2025
Calcium Signaling Group, Research Department, Weill Cornell Medicine Qatar, Education City, Qatar Foundation, Doha, Qatar.
The steroid hormone progesterone (P4) regulates multiple aspects of reproductive and metabolic physiology. Classical P4 signaling operates through nuclear receptors that regulate transcription. In addition, P4 signals through membrane P4 receptors (mPRs) in a rapid nongenomic modality.
View Article and Find Full Text PDFLife Med
April 2024
The State Key Laboratory for Complex Severe and Rare Diseases, SXMU-Tsinghua Collaborative Innovation Center for Frontier Medicine, Department of Basic Medical Sciences, School of Medicine, Tsinghua University, Beijing 100084, China.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!