Project description:B-1a cells are important immune cells and are the first line of defence against pathogens. During aging, B-1a cells undergo a series of changes that reduce their protective effects on the body. However, the characteristics of B-1a cells during aging are not fully understood. In this study, we transcriptionally and epigenetically characterised B-1a cells from 3-month-old and 24-month-old mice. Interestingly, we found that the expression of the transcription factor Bcl11a was positively correlated with the number of B-1a cells in old male and old female mice. We performed single-cell sequencing from C57BL/6 young female mice (3 months of age), middle-aged female mice (15 months of age) old female mice (26 months of age) to characterise the senescence transition in female mice.
Project description:B-1a cells are important immune cells, serving as the first line of defense against pathogens. B-1a cell undergo a series of alterations during aging and decrease the protection to our body. However, the characteristics of B-1a cells during the aging process are not fully understood. In this study, we discrible transcriptional and epigenetic profiles of B-1a from 3-month-old and 24-month-old mice across both genders. Interestingly，We found that the expression of the transcription factor Bcl11a was positively correlated with the number of B-1a cells in aged male and aged female mice.To further characterize senescent B-1a cells and the mechanisms of Bcl11a regulates B-1a. ATAC-seq and RNA-seq were performed on the B-1a isolated from young male mice (3-month-old),old male mice (24-month-old mice), young female mice (3-month-old),old female mice (24-month-old mice) of C57BL/6,and Bcl11a delated young male mice. CUT&tag was performed on the B-1a isolated from young male mice. Collectively, we provide a comprehensive resource to decode the aging process of B-1a, shedding light on how Bcl11a regulate B-1a cells maintenance.
Project description:B-1a cells are important immune cells, serving as the first line of defense against pathogens. B-1a cell undergo a series of alterations during aging and decrease the protection to our body. However, the characteristics of B-1a cells during the aging process are not fully understood. In this study, we discrible transcriptional and epigenetic profiles of B-1a from 3-month-old and 24-month-old mice across both genders. Interestingly，We found that the expression of the transcription factor Bcl11a was positively correlated with the number of B-1a cells in aged male and aged female mice.To further characterize senescent B-1a cells and the mechanisms of Bcl11a regulates B-1a. ATAC-seq and RNA-seq were performed on the B-1a isolated from young male mice (3-month-old),old male mice (24-month-old mice), young female mice (3-month-old),old female mice (24-month-old mice) of C57BL/6,and Bcl11a delated young male mice. CUT&tag was performed on the B-1a isolated from young male mice. Collectively, we provide a comprehensive resource to decode the aging process of B-1a, shedding light on how Bcl11a regulate B-1a cells maintenance.
Project description:B-1a cells are important immune cells, serving as the first line of defense against pathogens. B-1a cell undergo a series of alterations during aging and decrease the protection to our body. However, the characteristics of B-1a cells during the aging process are not fully understood. In this study, we discrible transcriptional and epigenetic profiles of B-1a from 3-month-old and 24-month-old mice across both genders. Interestingly，We found that the expression of the transcription factor Bcl11a was positively correlated with the number of B-1a cells in aged male and aged female mice.To further characterize senescent B-1a cells and the mechanisms of Bcl11a regulates B-1a. ATAC-seq and RNA-seq were performed on the B-1a isolated from young male mice (3-month-old),old male mice (24-month-old mice), young female mice (3-month-old),old female mice (24-month-old mice) of C57BL/6,and Bcl11a delated young male mice. CUT&tag was performed on the B-1a isolated from young male mice. Collectively, we provide a comprehensive resource to decode the aging process of B-1a, shedding light on how Bcl11a regulate B-1a cells maintenance.
