The goal of captive breeding programmes is often to maintain genetic diversity until re-introductions can occur. However, due in part to changes that occur in captive populations, approximately one-third of re-introductions fail. We evaluated genetic changes in captive populations using microsatellites and mtDNA. We analysed six populations of white-footed mice that were propagated for 20 generations using two replicates of three protocols: random mating (RAN), minimizing mean kinship (MK) and selection for docility (DOC). We found that MK resulted in the slowest loss of microsatellite genetic diversity compared to RAN and DOC. However, the loss of mtDNA haplotypes was not consistent among replicate lines. We compared our empirical data to simulated data and found no evidence of selection. Our results suggest that although the effects of drift may not be fully mitigated, MK reduces the loss of alleles due to inbreeding more effectively than random mating or docility selection. Therefore, MK should be preferred for captive breeding. Furthermore, our simulations show that incorporating microsatellite data into the MK framework reduced the magnitude of drift, which may have applications in long-term or extremely genetically depauperate captive populations.
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Introduction: China implemented a dynamic zero-COVID strategy to curb viral transmission in response to the coronavirus disease 2019 (COVID-19) pandemic. This strategy was designed to inhibit mutation of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for COVID-19. This study explores the dynamics of viral evolution under stringent non-pharmaceutical interventions (NPIs) through real-world observations.
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Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, 130122, People's Republic of China.
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Department of Urology, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, 730030, People's Republic of China.
Benign prostatic hyperplasia (BPH) is a prevalent urinary system disorder. Despite evidence of a significant genetic component from previous studies, the specific pathogenic genes and biological mechanisms are still largely unknown. The study utilized the FinnGen R10 dataset, encompassing 177,901 individuals (36,601 cases and 141,300 controls), and the GTEx v8 EQTLs files to conduct single-tissue and cross-tissue transcriptome-wide association studies (TWAS).
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Previous studies have found that dyslipidemia is a risk factor for pancreatic cancer (PC), and that lipid-lowering drugs may reduce the risk of PC. However, it is not clear whether dyslipidemia causes PC. The Mendelian randomization (MR) study aimed to investigate the causal role of lipid traits in pancreatic cancer and to assess the potential impact of lipid-lowering drug targets on pancreatic cancer.
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