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Many passerines have elaborated songs hypothesized to have evolved through sexual selection. Extra-pair mating can be a contributing factor in the evolution of complex songs by increasing the variance in male fitness. We investigated this by quantifying the relationship between male song performance and complexity and levels of paternity loss through extra-pair mating by their female mates in the grass wren (), a socially monogamous passerine with elaborate songs. We conducted fieldwork in the Uspallata Valley, Mendoza, Argentina over two breeding seasons and recorded the songs of 30 focal males during the egg-laying stage of their social mate. We collected blood samples from adults and nestlings and used ddRAD sequencing SNP data to determine parentage. We assessed the extra-pair mating behaviour of females by measuring paternity loss of their social partner and examined whether variation in paternity loss was associated with structural characteristics of that male's songs. We found relationships between paternity loss and song duration, syllable diversity and duty cycle. Our findings indicate that some specific traits of male song are associated with lower levels of paternity loss and therefore potentially higher fitness. Future studies should determine whether this relationship is a result of female preference (intersexual selection), effective male mate guarding or territory defence (intrasexual selection) or both.
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http://dx.doi.org/10.1098/rspb.2025.0241 | DOI Listing |
Stem Cell Rev Rep
September 2025
Stem Cells and Metabolism Research Program (STEMM), Research Programs Unit, Faculty of Medicine, University of Helsinki, Helsinki, 00014, Finland.
Mutations in Delta Like Non-Canonical Notch Ligand 1 (DLK1), a paternally expressed imprinted gene, underlie central precocious puberty (CPP), yet the mechanism remains unclear. To test the hypothesis that DLK1 plays a role in gonadotropin releasing hormone (GnRH) neuron ontogeny, 75 base pairs were deleted in both alleles of DLK1 exon 3 with CRISPR-Cas9 in human pluripotent stem cells (hPSCs). This line, exhibiting More than 80% loss of DLK1 protein, was differentiated into GnRH neurons by dual SMAD inhibition (dSMADi), FGF8 treatment and Notch inhibition, as previously described, however, it did not exhibit accelerated GNRH1 expression.
View Article and Find Full Text PDFCommun Biol
September 2025
UNC Neuroscience Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Angelman syndrome (AS) is a debilitating neurodevelopmental disorder caused by loss of maternally-inherited UBE3A. In neurons, paternally-inherited UBE3A is silenced in cis by a long non-coding RNA called Ube3a-ATS. Here, we found that Neisseria meningitidis Cas9 with two mutations (D15A and H587A) in the nuclease domains (dNmCas9) can unsilence the dormant paternal Ube3a allele in mouse and human neurons when targeted to Snord115 snoRNA genes located in introns of Ube3a-ATS.
View Article and Find Full Text PDFMol Cytogenet
August 2025
Assisted Reproduction Unit, Department of Obstetrics and Gynecology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310016, Zhejiang, China.
Background: Prader-Willi Syndrome (PWS) is a complicated genetic disorder demonstrating a variety of clinical phenotypes. Using molecular cytogenetics approaches to detect the deletions of the paternal 15q11-q13 region and maternal uniparental disomy of chromosome 15 plays an important role in the prenatal diagnosis of PWS.
Case Presentation: A pregnant woman with advanced maternal age underwent amniocentesis.
Nucleic Acids Res
August 2025
Roche Pharma Research and Early Development, Neuroscience and Rare Disease discovery and translational area, Roche Innovation Center Basel, Basel 4070, Switzerland.
Angelman syndrome (AS) is a severe neurodevelopmental disorder caused by the loss of neuronal ubiquitin E3 ligase UBE3A, with no available treatment. Restoring UBE3A by downregulating the paternally cis-acting long noncoding antisense transcript (UBE3A-ATS) is a potentially disease modifying strategy. However, developing molecules targeting human UBE3A-ATS is challenging due to its selective expression in mature neurons and lack of sequence conservation across species.
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