The BSDC1 Knockout HT29 Polyclonal Cells consist of a CRISPR/Cas9?edited polyclonal population of HT29 human colorectal adenocarcinoma cells bearing targeted disruption of the BSDC1 gene. This pool of edited cells provides a loss?of?function model for BSDC1, enabling functional dissection of its roles in chromatin biology and DNA damage response without single?cell clonal isolation.
The HT29 cell line originates from a primary colorectal adenocarcinoma of a 44?year?old female and is a widely used model for colorectal cancer research, intestinal epithelial physiology, and drug metabolism studies. These cells grow as adherent monolayers and carry key mutations characteristic of colorectal tumors, making them a relevant host for investigating BSDC1?dependent mechanisms in a disease context.
BSDC1 functions as a chromatin?associated factor that directly interacts with BPTF, a core subunit of the NURF remodeling complex, and with SMARCA4 to modulate nucleosome positioning at sites of DNA damage and gene regulatory regions. In the DNA damage response, BSDC1 is activated downstream of ATM/ATR kinases and the transcription factor E2F1, and it facilitates the recruitment of repair proteins such as BRCA1 and RAD51, promoting phosphorylation of H2AX (??H2AX). BSDC1 also impacts cell cycle progression by transcriptionally regulating CDKN1A (p21) and CCNB1 (cyclin B1), in part via p53? and MYC?dependent pathways. Thus, BSDC1 serves as a bridge between chromatin remodeling, DNA repair, and checkpoint control, with representative pathway members including ATM, CHK2, ??H2AX, p53, and the BPTF?NURF complex.
Loss of BSDC1 in HT29 cells impairs efficient DNA repair and disrupts cell cycle checkpoints, rendering the cells hypersensitive to genotoxic agents. This phenotype makes the knockout pool a powerful tool for colorectal cancer chemosensitivity screening, synthetic lethality studies, and mechanistic investigations of chromatin?mediated tumor suppression. The polyclonal composition preserves heterogeneity, allowing researchers to examine gene?dosage effects and adaptive responses.
Typical assays include western blotting for ??H2AX and p53, comet assay, flow cytometric cell cycle analysis, RT?qPCR of DNA repair genes, ChIP?qPCR for chromatin targets, and clonogenic survival assays. These cells support functional genomics screens, drug development, and basic research into DNA repair pathways. For further inquiries, please contact Ascent Research.
