Michael Bassik

Oct 2, 2024 | nature.com | Angela Pogson |Eric Sun |C. Tsui |Michael Bassik

AbstractAgeing impairs the ability of neural stem cells (NSCs) to transition from quiescence to proliferation in the adult mammalian brain. Functional decline of NSCs results in the decreased production of new neurons and defective regeneration following injury during ageing1,2,3,4. Several genetic interventions have been found to ameliorate old brain function5,6,7,8, but systematic functional testing of genes in old NSCs—and more generally in old cells—has not been done.

Aug 23, 2024 | nature.com | Christine Yeh |Olivia Laveroni |Subin Kim |Aihui Wang |Brooke Liang |Raeline Valbuena | +4 more

AbstractThe drivers of immune evasion are not entirely clear, limiting the success of cancer immunotherapies. Here we applied single-cell spatial and perturbational transcriptomics to delineate immune evasion in high-grade serous tubo-ovarian cancer. To this end, we first mapped the spatial organization of high-grade serous tubo-ovarian cancer by profiling more than 2.5 million cells in situ in 130 tumors from 94 patients.

Mar 19, 2024 | nature.com | David Yao |Josh Tycko |Lexi R. Bounds |Benjamin Doughty |Alexander White |Xingjie Ren | +16 more

AbstractThe ENCODE Consortium’s efforts to annotate noncoding cis-regulatory elements (CREs) have advanced our understanding of gene regulatory landscapes. Pooled, noncoding CRISPR screens offer a systematic approach to investigate cis-regulatory mechanisms. The ENCODE4 Functional Characterization Centers conducted 108 screens in human cell lines, comprising >540,000 perturbations across 24.85 megabases of the genome.

Sep 27, 2023 | nature.com | Xiangling Meng |Kent Imaizumi |Noah Reis |Michael Bassik

AbstractThe assembly of cortical circuits involves the generation and migration of interneurons from the ventral to the dorsal forebrain1,2,3, which has been challenging to study at inaccessible stages of late gestation and early postnatal human development4.

Sep 11, 2023 | nature.com | Blake Nelson |Nathan Livingston |Timothy J. Stasevich |Michael Bassik |Shuying Sun

AbstractC9ORF72 hexanucleotide repeat expansion is the most common genetic cause of both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). One pathogenic mechanism is the accumulation of toxic dipeptide repeat (DPR) proteins like poly-GA, GP and GR, produced by the noncanonical translation of the expanded RNA repeats. However, how different DPRs are synthesized remains elusive.