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Biology subjects

Parnika, S.

Publications and source records attributed to Parnika, S..

2 recordsLinked to original sources

Genome-scale prediction of context-specific synthetic lethality beyond protein interaction networks

Identifying synthetic lethal (SL) interactions offers a principled framework for discovering disease-specific therapeutic targets. However, current machine learning approaches heavily rely on curated protein-protein interaction networks. Because these networks cover only [~]7,500 proteins, they severely restrict the search space of human gene pairs and introduce systematic biases toward well-characterized genes. To circumvent these limitations, we developed SLxGO, a network-independent machine learning framework that predicts SL interactions directly from semantic representations of Gene Ontology annotations encoded via BioBERT-derived embeddings. Benchmarked across multiple cross-validation schemes against eight state-of-the-art methods, SLxGO consistently achieved superior predictive ranking performance, maintaining robustness under cold-start conditions for previously unseen genes. Integrating cell line-specific transcriptional profiles extended this framework to context-dependent SL prediction across six distinct cell lines. Notably, we experimentally confirmed a context-specific EFNA1-SLC29A1 SL interaction in HeLa cells, alongside synergistic pharmacological validation of an ACVR1-SLC29A1 vulnerability. All predictions are hosted on SLiGO, an open-access database encompassing 30 million human gene pairs, establishing a comprehensive, genome-scale resource for context-specific vulnerability mapping across the human interactome.

systems biology↗

A Comparative Chemical-Genetic Screen Reveals Divergent Roles for Host ALK2 Signaling Across Intracellular Bacterial Niches

Diverse vacuolar architectures present unique signaling challenges for intracellular bacteria, yet whether distinct niches share host requirements remains unclear. Because host kinases coordinate these complex cellular responses, we performed a comparative chemical-genetic screen of Coxiella burnetii, Chlamydia trachomatis, and Salmonella enterica. The screen revealed that C. burnetii is uniquely dependent on host kinase pathways. Deconvolution of these inhibitor profiles identified the bone morphogenetic protein (BMP) type I receptor, ALK2, as a critical regulatory checkpoint. While C. burnetii activates ALK2-mediated phospho-SMAD1/5/9 signaling to support replication, C. trachomatis actively suppresses this cascade. Mechanistically, ALK2 functions upstream of TFEB nuclear translocation and LAMP1 recruitment, driving the lysosomal biogenesis required to sustain the phagolysosome-like niche of C. burnetii while disrupting the non-lysosomal inclusion of C. trachomatis. Consequently, targeting ALK2 switches replication outcomes, demonstrating how distinct niches implement opposing strategies to exploit a single host signaling node.

microbiology↗