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Lin, S.-W.

Publications and source records attributed to Lin, S.-W..

2 recordsLinked to original sources

Diversification through sexual selection on gustatorial courtship traits in dwarf spiders

Sexual dimorphism can evolve under sexual selection or ecological factors. Sexually dimorphic male prosomal modifications are associated with gustatorial courtship in erigonines. The modifications vary from moderate elevations to bizarre shapes. Males transfer substances from these structures to females, which affect mate acceptance and fecundity. Here, we explore lability of these traits by investigating if modified prosomata are inherently linked to secretory glands, if glands evolved prior to prosomal modifications, and the possibility of convergent evolution and cryptic differentiation, aiming at assessing the possible role of this trait complex in speciation. We reconstructed the positions of glands and the musculature in the anterior part of prosomata of 76 erigonines and three outgroups using micro-CT. We incorporated these characters into an existing morphological character matrix and reanalyzed the phylogeny. Our results support the possession of glands as the ancestral state. The manifold modifications of the prosomal shape have evolved convergently. Differences in glandular positions between species with modified/unmodified prosomata suggest high lability of these traits. Cases of gland loss suggest considerable costs of gustatorial courtship. Our findings demonstrate divergent evolutionary patterns of these traits, and a likely facilitating effect of this type of sexual selection on speciation.

evolutionary biology↗

Toward the pathogenicity of the SLC26A4 p.C565Y variant using a genetically driven mouse model

Recessive variants of the SLC26A4 gene are a common cause of hearing impairment worldwide. In the past, cell lines and transgenic mice have been widely used to investigate the pathogenicity associated with the SLC26A4 variants. However, discrepancies in the pathogenicity between humans and cell lines or transgenic mice have been documented for some of the SLC26A4 variants. For instance, the p.C565Y variant, which has been reported to be pathogenic in humans, did not exhibit functional pathogenic consequences in cell lines. To address the pathogenicity of p.C565Y, we used a genotype-based approach in which we generated knock-in mice heterozygous (Slc26a4+/C565Y), homozygous (Slc26a4C565Y/C565Y), and compound heterozygous (Slc26a4919-2A>G/C565Y) for this variant. Subsequent phenotypic characterization revealed that mice segregating these genotypes demonstrated normal auditory and vestibular functions and normal inner ear morphology and expression of pendrin. These findings indicate that the p.C565Y variant is non-pathogenic for mice and that a single p.C565Y allele is sufficient to maintain normal inner ear physiology in mice. Our results highlight the differences in the pathogenicity associated with certain SLC26A4 variants between transgenic mice and humans, which should be taken into consideration while interpreting the results of animal studies for SLC26A4-related deafness.

genetics↗