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Rowley, J.

Publications and source records attributed to Rowley, J..

2 recordsLinked to original sources

Predicting A/B compartments from histone modifications using deep learning

Genomes fold into organizational units in the 3D space that can influence critical biological functions. In particular, the organization of chromatin into A and B compartments segregates its active regions from inactive regions. Compartments, evident in Hi-C contact matrices, have been used to describe cell-type specific changes in the A/B organization. However, obtaining Hi-C data for all cell and tissue types of interest is prohibitively expensive, which has limited the widespread consideration of compartment status. We present a prediction tool called Compartment prediction using Recurrent Neural Network (CoRNN) that models the relationship between the compartmental organization of the genome and histone modification enrichment. Our model predicts A/B compartments, in a cross-cell type setting, with an average area under the ROC curve of 90.9%. Our cell type-specific compartment predictions show high overlap with known functional elements. We investigate our predictions by systematically removing combinations of histone marks and find that H3K27ac and H3K36me3 are the most predictive marks. We then perform a detailed analysis of loci where compartment status cannot be accurately predicted from these marks. These regions represent chromatin with ambiguous compartmental status, likely due to variations in status within the population of cells. These ambiguous loci also show highly variable compartmental status between biological replicates in the same GM12878 cell type. Finally, we demonstrate the generalizability of our model by predicting compartments in independent tissue samples. Our software and trained model are publicly available at https://github.com/rsinghlab/CoRNN.

bioinformatics↗

Progressive and predictive markers of disease evolution: platelet transcriptome in chronic myeloproliferative neoplasms

Predicting disease progression remains a particularly challenging endeavor in chronic degenerative disorders and cancer, thus limiting early detection, risk stratification, and preventive interventions. Here, profiling the spectrum of chronic myeloproliferative neoplasms (MPNs) as a model, we identify the blood platelet transcriptome as a proxy for highly sensitive progression biomarkers that also enables prediction of advanced disease via machine learning algorithms. Using RNA sequencing (RNA-seq), we derive disease-relevant gene expression in purified platelets from 120 peripheral blood samples constituting two time-separated cohorts of patients diagnosed with one of three MPN subtypes at sample acquisition - essential thrombocythemia, ET (n=24), polycythemia vera, PV (n=33), and primary or post ET/PV secondary myelofibrosis, MF (n=42), and healthy donors (n=21). The MPN platelet transcriptome reveals an incremental molecular reprogramming that is independent of patient driver mutation status or therapy and discriminates each clinical phenotype. Leveraging this dataset that shows a characteristic progressive expression gradient across MPN, we develop a machine learning model (Lasso-penalized regression) and predict advanced subtype MF at high accuracy and under two conditions of external validation: i) temporal: our two Stanford cohorts, AUC-ROC of 0.96; and ii) geographical: independently published data of an additional n=25 MF and n=46 healthy donors, AUC-ROC of 0.97). Lasso-derived signatures offer a robust core set of < 5 MPN transcriptome markers that are progressive in expression. Mechanistic insights from our data highlight impaired protein homeostasis as a prominent driver of MPN evolution, with persistent integrated stress response. We also identify JAK inhibitor-specific signatures and other interferon, proliferation, and proteostasis-associated markers as putative targets for MPN-directed therapy. Our platelet transcriptome snapshot of chronic MPNs demonstrates a proof of principle for disease risk stratification and progression beyond genetic data alone, with potential utility in other progressive disorders. HighlightsLeveraging two independent and mutually validating MPN patient cohorts, we identify progressive transcriptomic markers that also enable externally validated prediction in MPNs. Our platelet RNA-Seq data identifies impaired protein homeostasis as prominent in MPN progression and offers putative targets of therapy. VISUAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=135 HEIGHT=200 SRC="FIGDIR/small/435190v3_ufig1.gif" ALT="Figure 1"> View larger version (42K): org.highwire.dtl.DTLVardef@72dc16org.highwire.dtl.DTLVardef@cf5096org.highwire.dtl.DTLVardef@b3d460org.highwire.dtl.DTLVardef@3c0ddc_HPS_FORMAT_FIGEXP M_FIG C_FIG

genomics↗