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Ravi Sundar Jose Geetha, A.

Publications and source records attributed to Ravi Sundar Jose Geetha, A..

2 recordsLinked to original sources

Differences between in vivo and ex vivo hematopoietic model systems modulate the outcomes of genetic perturbations.

Ex vivo experimental models are extensively used as reductionist models, yet the impact of model choice on molecular states and perturbation responses has not been systematically evaluated. Here, we compared the outcomes of genetic perturbations in hematopoietic stem cells between in vivo and ex vivo model systems. This revealed strong baseline differences characterized by a reduced interferon response and elevated growth and metabolism signatures in ex vivo models, a pattern recapitulated in various orthogonal human and mouse systems. We further found substantial differences between perturbation effects between in vivo and ex vivo models, with some perturbations showing opposite effects. Finally, we evaluated whether AI-based perturbation prediction models can predict in vivo perturbation effects from ex vivo perturbation effects, which proved challenging. Together, our findings reveal systematic biases in ex vivo models, demonstrate how these biases influence perturbation outcomes, suggest approaches to enhance ex vivo systems, and provide a test case for computational prediction of perturbation effects.

systems biology↗

Dynamic control of gene expression by ISGF3 and IRF1 duringIFNbeta and IFNgamma signaling

Type I interferons (IFN-I, including IFN{beta}) and IFN{gamma} produce overlapping, yet clearly distinct immunological activities. Recent data show that distinctness of global transcriptional responses to the two IFN types is not apparent when comparing their immediate effects. By analyzing nascent transcripts induced by IFN-I or IFN{gamma} over a period of 48hrs we now show that the distinctiveness of the transcriptomes emerges over time and is based on a different employment of the ISGF3 complex as well as the second-tier transcription factor IRF1. The distinct transcriptional properties of ISGF3 and IRF1 correspond with a largely diverse nuclear protein interactome. Mechanistically, we describe specific input of ISGF3 and IRF1 into enhancer activation and the regulation of chromatin accessibility at interferon-induced genes (ISG). We further report differences between the IFN types in altering RNA polymerase II pausing at ISG 5 ends. Our data provide insight how transcriptional regulators create immunological identities of IFN-I and IFN{gamma}.

immunology↗