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Biology subjects

Heydari, H.

Publications and source records attributed to Heydari, H..

6 recordsLinked to original sources

Semantic fragment representations for coordinate-free analysis of genomics data

Many genomic assays begin with individual DNA fragments, but standard analysis quickly collapses those molecules into counts over genomic intervals. Rich information carried by each fragment, including its sequence, fragment body, cleavage boundaries, and local flanking context, is lost in this process. This loss is especially apparent in mixed-source and heterogeneous samples, where individual fragments originate from disparate cell types and can retain information about their cell of origin. To address this, we present LEAF-1, a fragment-level foundation model pre-trained on approximately 58 billion fragments spanning bulk ATAC-seq, single-cell ATAC-seq, and cell-free DNA profiles, representing each DNA molecule as a point in a learned semantic space defined by sequence context, assay modality, and explicit cleavage-boundary tokens. In sparse scATAC-seq datasets, mean-pooled LEAF-1 embeddings readily classify human cell types from as few as [~]1,000 fragments per cell, with high-scoring fragments linked to cell-type-associated transcription-factor programs. Similarly, in cell-free DNA profiling, LEAF-1 outperformed state-of-the-art coordinate-binning strategies and general-purpose DNA language model baselines across cancer detection tasks. Applying attention-based multiple-instance learning to LEAF-1 embeddings further improved cancer detection, reaching an area under the receiver operating characteristic (ROC) curve (AUC) of 0.95. This pan-cancer model generalizes beyond cancer types it is trained on, as we show by profiling plasma samples from clear cell renal cell carcinoma patients and healthy volunteers and applying the frozen classifier without retraining, achieving an AUC of 0.83. These results show that semantic learning over individual DNA fragments preserves biochemical, cell-associated, and disease-associated signals that are otherwise lost during coordinate-based aggregation.

genomics↗

Back to basics: Observed statistics are sufficient to predict drug responses

Predicting how cells, tissues, and patients will respond to a drug, cytokine, or genetic perturbation is central to biological and clinical reasoning. The practical goal is to estimate the analysis-ready readouts that support this reasoning: which cellular responses are context-dependent, which perturbations reveal shared or divergent mechanisms, and which observations should become the basis for the next experiment. Here we introduce Rhaister, a perturbation-response predictor that operates directly on screen-level summary statistics. By measuring just a few perturbations in a new biological context, Rhaister predicts the unmeasured perturbations by learning how response patterns vary across reference contexts. This formulation applies to both fine-grained molecular readouts, such as transcriptional responses from Tahoe-100M or other large perturbation screen, or on phenotypic endpoints. To train and apply Rhaister on pheno-typic endpoints we created Emerald Bay, a purpose-built Tahoe dataset that unifies multi-day cancer drug perturbation, pooled Mosaic tumor contexts, and paired transcriptomic response measurements*. Across these settings, Rhaister matches or exceeds substantially more expensive virtual-cell models, often achieving the highest values possible in evaluation metrics, while training in seconds and running predictions in milliseconds. On Emerald Bay, Rhaister predicts context-specific drug phenotypes from sensitivity measurements alone and improves further when including transcriptomic information. We also introduce Rhaister-O, predicting drug responses in new contexts from baseline expression alone and, to our knowledge, provides the first zero-shot model for this task. Rhaister establishes summary-statistic perturbation modeling as a fast, interpretable framework for predicting biological response across new contexts.

genomics↗

FLASH-MM: fast and scalable single-cell differential expression analysis using linear mixed-effects models

Single-cell RNA sequencing (scRNA-seq) enables detailed comparisons of gene expression across cells and conditions. Single-cell differential expression analysis faces challenges like sample correlation, individual variation, and scalability. We developed a fast and scalable linear mixed-effects model (LMM) estimation algorithm, FLASH-MM, to address these issues. We reformulate aspects of the linear mixed model estimation procedure to make it faster, by reducing computational complexity and memory use in the case of working with a gene by cell matrix. Simulation studies with scRNA-seq data show that FLASH-MM is accurate, computationally efficient, effectively controls false positive rates, and maintains high statistical power in differential expression analysis. Tests on tuberculosis immune and kidney single cell data demonstrate FLASH-MMs utility in accelerating single-cell differential expression analysis across diverse biological contexts.

bioinformatics↗

Parameterization of intraoperative human microelectroderecordings: Linking action potential morphology to brainanatomy

Deep brain stimulation (DBS) is a targeted manipulation of brain circuitry to treat neurological and neuropsychiatric conditions. Optimal DBS lead placement is essential for treatment efficacy. Current targeting practice is based on preoperative and intraoperative brain imaging, intraoperative electrophysiology, and stimulation mapping. Electrophysiological mapping using extracellular microelectrode recordings aids in identifying functional subdomains, anatomical boundaries, and disease-correlated physiology. The shape of single-unit action potentials may differ due to different biophysical properties between cell-types and brain regions. Here, we describe a technique to parameterize the structure and duration of sorted spike units using a novel algorithmic approach based on canonical response parameterization, and illustrate how it may be used on DBS microelectrode recordings. Isolated spike shapes are parameterized then compared using a spike similarity metric and grouped by hierarchical clustering. When spike morphology is associated with anatomy, we find regional clustering in the human globus pallidus. This method is widely applicable for spike removal and single-unit characterization and could be integrated into intraoperative array-based technologies to enhance targeting and clinical outcomes in DBS lead placement. Author summaryWe developed a new algorithmic approach to capture the structure of single neuron electrophysiology from microelectrode recordings during deep brain stimulation surgery. This method has broad applications for spike characterization, clustering, removal from the background field potential, and comparison across recording sites. Using this technique, we illustrate regional clustering of spike morphologies in the human globus pallidus.

neuroscience↗

Refining the resolution of the yeast genotype-phenotype map using single-cell RNA-sequencing

Genotype-phenotype mapping (GPM), or the association of trait variation to genetic variation, has been a long-lasting problem in biology. The existing approaches to this problem allowed researchers to partially understand within- and between-species variation as well as the emergence or evolution of phenotypes. However, traditional GPM methods typically ignore the transcriptome or have low statistical power due to challenges related to dataset scale. Thus, it is not clear to what extent selection modulates transcriptomes and whether cis- or trans-regulatory elements are more important. To overcome these challenges, we leveraged the cost efficiency and scalability of single-cell RNA sequencing (scRNA-seq) by collecting data from 18,233 yeast cells from 4,489 F2 segregants derived from an F1 cross between the laboratory strain BY4741 and the vineyard strain RM11-1a. More precisely, we performed eQTL mapping with the scRNA-seq data to identify single-cell eQTL (sc-eQTL) and transcriptome variation patterns associated with fitness variation inferred from the segregant bulk fitness assay. Due to the larger scale of our dataset and its multidimensionality, we could recapitulate results from decades of work in GPM from yeast bulk assays while revealing new associations between phenotypic and transcriptomic variations at a broad scale. We evaluated the strength of the association between phenotype variation and expression variation, revealed new hotspots of gene expression regulation associated with trait variation, revealed new gene functions with high expression heritability, and highlighted the larger aggregate effect of trans-regulation compared to cis-regulation. Altogether, these results suggest that integrating large-scale scRNA-seq data into GPM improves our understanding of trait variation in the context of transcriptomic regulation.

evolutionary biology↗

Discovering genetic interactions bridging pathways in genome-wide association studies

Genetic interactions have been reported to underlie phenotypes in a variety of systems, but the extent to which they contribute to complex disease in humans remains unclear. In principle, genome-wide association studies (GWAS) provide a platform for detecting genetic interactions, but existing methods for identifying them from GWAS data tend to focus on testing individual locus pairs, which undermines statistical power. Importantly, the global genetic networks mapped for a model eukaryotic organism revealed that genetic interactions often connect genes between compensatory functional modules in a highly coherent manner. Taking advantage of this expected structure, we developed a computational approach called BridGE that identifies pathways connected by genetic interactions from GWAS data. Applying BridGE broadly, we discovered significant interactions in Parkinsons disease, schizophrenia, hypertension, prostate cancer, breast cancer, and type 2 diabetes. Our novel approach provides a general framework for mapping complex genetic networks underlying human disease from genome-wide genotype data.

genetics↗