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1.
Sci Rep ; 13(1): 7388, 2023 05 06.
Artigo em Inglês | MEDLINE | ID: mdl-37149712

RESUMO

Deciphering the origins of phenotypic variations in natural animal populations is a challenging topic for evolutionary and conservation biologists. Atypical morphologies in mammals are usually attributed to interspecific hybridisation or de-novo mutations. Here we report the case of four golden jackals (Canis aureus), that were observed during a camera-trapping wildlife survey in Northern Israel, displaying anomalous morphological traits, such as white patches, an upturned tail, and long thick fur which resemble features of domesticated mammals. Another individual was culled under permit and was genetically and morphologically examined. Paternal and nuclear genetic profiles, as well as geometric morphometric data, identified this individual as a golden jackal rather than a recent dog/wolf-jackal hybrid. Its maternal haplotype suggested past introgression of African wolf (Canis lupaster) mitochondrial DNA, as previously documented in other jackals from Israel. When viewed in the context of the jackal as an overabundant species in Israel, the rural nature of the surveyed area, the abundance of anthropogenic waste, and molecular and morphological findings, the possibility of an individual presenting incipient stages of domestication should also be considered.


Assuntos
Canidae , Lobos , Cães , Animais , Chacais/genética , Lobos/genética , Domesticação , Evolução Biológica
2.
Front Med (Lausanne) ; 7: 582793, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33195331

RESUMO

Diverse populations worldwide are differentially affected by coronavirus disease 2019 (COVID-19). While socioeconomic background has been studied extensively, little is known about the genetic variation underlying this phenomenon. This study is aimed at examining the genetic basis behind the great discrepancies among diverse ethnic groups in terms of COVID-19 susceptibility for viral infection, disease prognosis, and mortality. To this end, in silico analysis of single-nucleotide polymorphisms (SNPs) within regulatory sequences of the human angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2)-the virus's gateway to host cells-and their plausible implications on expression levels was conducted. We provide indication that the variation in the human ACE2 and TMPRSS2 regulatory sequences is likely to be involved in and contribute to this phenomenon. SNPs that are abundant in the more susceptible populations introduce binding sites (BSs) for transcription factors or they may invalidate BSs for transcription repressor-both may enhance target gene (ACE2 or TMPRSS2) expression in the relevant target tissues. SNPs that are abundant in the more resistant populations may invalidate BSs for a transcriptional repressor or they may introduce BSs for a transcriptional repressor or initiator of mRNA degradation, which may reduce target gene expression levels. This aspect, when added to the socioeconomic factors, can be a cause for the divergent prevalence of the disease and the different mortality rates within diverse populations. This demonstration may call for a shift in the paradigm of searching for COVID-19 biomarkers, such that SNPs within regulatory sequences should be of high importance.

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