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Polonsky, M.

Publications and source records attributed to Polonsky, M..

3 recordsLinked to original sources

Spatial second-order features predict glioma malignant transformation

Isocitrate dehydrogenase (IDH) mutant gliomas often transform from low to high grade aggressive tumors. The genetic and molecular drivers of this Malignant Transformation (MT) are poorly understood, and predicting whether a patient will undergo MT is an unmet challenge of high clinical relevance. To stratify patients by MT risk, we applied integrated spatial DNA and RNA profiling to biopsies from 18 retrospective glioma patients which will either remain stable, undergo MT or have already transformed. The resulting dataset consisted of >600,000 single cells, measuring 962 DNA loci, 1150 RNAs, and their spatial locations. Using this dataset, we found that genetic copy number alterations (CNAs), cell types compositions, and cellular neighborhoods did not predict MT. Instead, second order effects i.e. pairwise interactions, are highly predictive of future transformation. First, we identified abnormal chromosomal contact patterns that clearly separate future stable versus future MT samples. Second, we identified 24 ligand-receptors (LR) pairs cross-expressed in neighboring cells as the main molecular factors predictive of transformation and recurrences. We then validated a cross-expressing pair of ENPP2-LPAR1 interactions with a separate cohort of patient samples. In addition, using the LR+ cell pairs as an anchor, we identified cell signaling-specific gene expression programs that can predict from bulk or single cell RNAseq data the time to recurrence. We used a cell-interaction-based foundation model (CIFM) optimized on the spatial RNA data in forward simulations and identified potential myeloid signaling factors involved in MT. Lastly, we analyzed the effect of detection sensitivity on the ability to capture pertinent LR+ neighboring cells by down-sampling transcript and showed that the ability to detect cross-expressing signaling LR transcripts (typically <10 copies per cell) decays rapidly with lower sensitivity, but is more robust to down-sampling of the areas of the tissue imaged. The importance of second-order features suggests that increased depth and dimensionality of data on a smaller quantity of samples can provide valuable insight, and that high-sensitivity and multiple-modalities spatial approaches can help identify markers to risk-stratify patients, aid in therapeutic decision making, and uncover potential therapeutic targets.

cancer biology↗

Spatial transcriptomics defines injury-specific microenvironments in the adult mouse kidney and novel cellular interactions in regeneration and disease

Kidney injury disrupts the intricate renal architecture and triggers limited regeneration, and injury-invoked inflammation and fibrosis. Deciphering molecular pathways and cellular interactions driving these processes is challenging due to the complex renal architecture. Here, we applied single cell spatial transcriptomics to examine ischemia-reperfusion injury in the mouse kidney. Spatial transcriptomics revealed injury-specific and spatially-dependent gene expression patterns in distinct cellular microenvironments within the kidney and predicted Clcf1-Crfl1 in a molecular interplay between persistently injured proximal tubule cells and neighboring fibroblasts. Immune cell types play a critical role in organ repair. Spatial analysis revealed cellular microenvironments resembling early tertiary lymphoid structures and identified associated molecular pathways. Collectively, this study supports a focus on molecular interactions in cellular microenvironments to enhance understanding of injury, repair and disease. One-Sentence Summary: Spatial transcriptomics predicted a molecular interplay amongst neighboring cell-types in the injured mammalian kidney Main Text:

molecular biology↗

Dynamic changes in tRNA modifications and abundance during T-cell activation

The tRNA pool determines the efficiency, throughput, and accuracy of translation. Previous studies have identified dynamic changes in the tRNA supply and mRNA demand during cancerous proliferation. Yet, dynamic changes may occur also during physiologically normal proliferation, and these are less characterized. We examined the tRNA and mRNA pools of T-cells during their vigorous proliferation and differentiation upon triggering their antigen receptor. We observe a global signature of switch in demand for codons at the early proliferation phase of the response, accompanied by corresponding changes in tRNA expression levels. In the later phase, upon differentiation, the response of the tRNA pool is relaxed back to basal level, potentially restraining excessive proliferation. Sequencing of tRNAs allowed us to also evaluate their diverse base-modifications. We found that two types of tRNA modifications, wybutosine and ms2t6A, are reduced dramatically during T-cell activation. These modifications occur in the anti-codon loops of two tRNAs that decode "slippery codons", that are prone to ribosomal frameshifting. Attenuation of these frameshift-protective modifications is expected to increase the potential for proteome-wide frameshifting during T-cell proliferation. Indeed, human cell lines deleted of a wybutosine writer showed increased ribosomal frameshifting, as detected with a HIV gag-pol frameshifting site reporter. These results may explain HIVs specific tropism towards proliferating T-Cells since it requires ribosomal frameshift exactly on the corresponding codon for infection. The changes in tRNA expression and modifications uncover a new layer of translation regulation during T-cell proliferation and exposes a potential trade-off between cellular growth and translation fidelity. Significance statementThe tRNA pool decodes genetic information during translation. As such, it is subject to intricate physiological regulation in all species, across different physiological conditions. Here we show for the first time a program that governs the tRNA pool and its interaction with the transcriptome upon a physiological cellular proliferation- T-cells activation. We found that upon antigenic activation of T-cells, their tRNA and mRNA pools undergo coordinated and complementary changes, which are relaxed when cells reduce back their proliferation rate and differentiate into memory cells. We found a reduction in two particular tRNA modifications that have a role in governing translation fidelity and frameshift prevention. This exposes a vulnerability in activated T-cells that may be utilized by HIV for its replication. ClassificationBIOLOGICAL SCIENCES; cell biology

genomics↗