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Chromosome-level genome assemblies of 11 bamboo species comprising lineages from diploid (herbaceous) to tetraploid and hexaploid (woody) provide insights into dynamic subgenome dominance in bamboos.
We show that in addition to promoter activation, MYC drives cancer progression by activating transcriptional enhancers via a distinct mechanism. MYC cooperates with several other proteins at these cis-regulatory regions to change the epigenome and promote recruitment of RNA polymerase II and enhancer transcription.
Analysis of enhancer–promoter (E–P) interactions during Drosophila embryogenesis suggests that the relationship between E–P proximity and activity depends on the developmental stage. Increased E–P proximity is associated with activity during differentiation but not specification.
Mutational signatures help to deconvolve the different processes that shape cancer genomes. A new tool now alleviates some of the persistent challenges in the field.
This paper highlights the mechanisms underlying MYC-dependent gene regulation from transcriptional enhancers, which are distinct to the function of MYC at promoters. This process takes place in a cancer type-specific way, and the resulting transcriptional programs can predict prognosis.
Digenic inheritance of deleterious variants in serine/arginine protein kinase 3 (SRPK3) and titin (TTN) leads to a progressive early onset skeletal muscle myopathy. Zebrafish double mutants exhibit a similar myopathy phenotype accompanied by myofibrillar disorganization.
Epigenetic profiles can be predictive of macrophage transcriptional responses to influenza A virus infection in individuals of European and African ancestry. Ancestry-linked epigenetic differences appear to be genetically controlled.
An approach combining infection of primary human epithelial cells with a barcoded lentiviral-based library followed by engraftment into mice yields biologically relevant models of bladder and prostate cancer harboring complex genetic perturbations.
Genome-wide CRISPR screening coupled with ATAC-see uncovered modulators that influence global chromatin accessibility. Notably, TFDP1 emerged as a pivotal modulator of chromatin accessibility that acts by controlling histone transcription. Depletion of TFDP1 induced a global elevation in accessibility, enhancing the efficiency of genome editing and iPS cell reprogramming.
Gestational diabetes is a complex metabolic condition thought to have a strong genetic predisposition. A large genome-wide association study of participants from Finland sheds light on the genetic contributors, opening avenues for research into mechanisms that underlie glucose regulation in pregnancy to improve the health of mothers and babies.
Spatial omics enables the molecular profiling of cells with the tissue context preserved. A new analytic approach shows how cellular neighborhood analysis and feature augmentation can spatially connect and cluster millions of cells into higher-order functional units.
BANKSY is an algorithm with R and Python implementations that identifies both cell types and tissue domains from spatially resolved omics data by incorporating spatial kernels capturing microenvironmental information. It is applicable to a range of technologies and is scalable to millions of cells.
This study examines karyotypic selection and evolution in vitro using immortalized mammary and kidney epithelial cell lines, observing aneuploidy patterns specific to each origin tissue that are correlated with frequencies in patient tumors and independent of drivers such as TP53 mutation.