Project description:The genetic foundation of chicken tail feather color is not very well studied to date, though that of body feather color is extensively explored. In the present study, we used a synthetic chicken dwarf line (DW), which was originated from the hybrids between a black tail chicken breed, Rhode Island Red (RIR) and a white tail breed, Dwarf Layer (DL), to understand the genetic rules of the white/black tail color. The DW line still contain the individuals with black or white tails, even if the body feather are predominantly red, after more than ten generation of self-crossing and being selected for the body feather color. We firstly performed four crosses using the DW line chickens including black tail male to female, reciprocal crosses between the black and white, and white male to female to elucidate the inheritance pattern of the white/black tail. We found that (i) the white/black tail feather colors are independent of body feather color and (ii) the phenotype are autosomal simple trait and (iii) the white are dominant to the black in the DW lines. Furtherly, we performed a genome-wide association (GWA) analysis to determine the candidate genomic regions underlying the tail feather color by using black tail chickens from the RIR and DW chickens and white individuals from DW lines.
Project description:we compared the skin transcriptomes of the black- and white-coated region from the Boer and Macheng Black crossbred goat with black head and white body using the Illumina RNA-Seq method. Six cDNA libraries derived from skin samples of the white coat region (n = 3) and black coat region (n = 3) were constructed from three full-sib goats. On average, we obtained approximately 76.5 and 73.5 million reads for each skin sample of black coat and white coat, respectively, of which 75.39% and 76.05% reads were covered in the genome database. Our study provides insight into the transcriptional regulation of two distinct coat color that might serve as a key resource for understanding coat color pigmentation of goat.
Project description:Genomic profiles and prognostic biomarkers in patients with acute myeloid leukemia (AML) from ancestry diverse populations are underexplored. We analyzed the exomes and transcriptomes of 100 Black patients with AML (Alliance) and compared somatic mutation frequencies with those of 323 White patients (BeatAML). Seventy-three percent of 162 recurrent gene mutations identified in Black patients, including a novel PHIP alteration detected in 7% of patients, were found in only ≤1 White patient. Black patients with myelodysplasia-related AML were younger than White patients suggesting intrinsic and/or extrinsic dysplasia-causing stressors. On multivariable outcome analyses of Black patients, NPM1 and NRAS mutations associated with inferior disease-free and IDH1/2 mutations with reduced overall survival. Inflammatory profiles, cell type distributions and transcriptional profiles differed between Black and White NPM1-mutated patients. Incorporation of ancestry-specific risk markers into the 2022 European LeukemiaNet genetic-risk stratification changed risk-group assignment for one-third of Black patients and improved their outcome prediction.
Project description:Influence of copy number changes at several chromosomes to melanin production and virulence of Cryptococcus neoformans Black(B4) and white(W2) strains were compared to each other. Black variant from white strain (W2BA1) is also compared to the black strain(B4).
Project description:Hepatocellular carcinoma (HCC) is a highly fatal disease with mortality running parallel to its incidence. For HCC patients, there is a statistically significant increase in incidence and mortality and a decrease in 5-year survival rates in African American (AA)/Black patients compared to non-Hispanic (white) patients. There is a gap of knowledge in our understanding of the molecular mechanism underlying the HCC racial disparity between AA/Black and white patients. To address this issue, we analyzed existing RNA-sequencing (RNA-seq) data from HCC patients in the TCGA database, and performed RNA-seq in 14 white and 19 AA/Black HCC patients from Virginia Commonwealth University. In both analysis the only pathway which showed statistically significant activation in AA/Black patients, compared to white patients, was type I interferon (IFN-I) signaling. A four gene signature of IFN-I-stimulated genes (ISGs) showed increased expression in AA/Black HCC tumors compared to their white counterparts. HCC is a disease of chronic inflammation and IFN-I function as a pro-inflammatory and immunosuppressive cytokine. These findings suggest a potential role of IFN-I in conferring disparity in AA/Black HCC patients.