Skip to main content
Premium Trial:

Request an Annual Quote

Cell Studies on CCLE Proteomics, Toxoplasma Parasite Differentiation, Autism-Related Genes

Researchers from Harvard Medical School, the Novartis Institutes for Biomedical Research, Broad Institute, and other centers present a quantitative proteomic atlas produced from hundreds of Cancer Cell Line Encyclopedia (CCLE) lines. By generating multiplexed, mass spectrometry-based proteomic profiles for 375 cell lines, the team characterized protein levels in lines with or without microsatellite instability or other alterations, while uncovering co-expressed genes and proteins from distinct pathways, proteins or pathways with recurrent dysregulation in the cancer cells, and potential gene or protein targets. The authors note that the new proteomic data complement available genetic insights on the CCLE collection, providing "a broad resource to explore cellular behavior and facilitate cancer research."
A team from the Whitehead Institute for Biomedical Research, the Massachusetts Institute of Technology, and elsewhere looks at gene regulation and differentiation in the single-celled eukaryotic parasite Toxoplasma gondii, which causes intracellular infections and corresponding cysts. Using gene editing, a reporter screen, single-cell RNA-seq, and other approaches, the researchers focused in on and characterized the transcription BFD1, which they call a master regulator of differentiation in Toxoplasma parasites from chronic-stage infections. "Collectively, modulation of BFD1 holds substantial clinical and biotechnological potential, as chronic infection represents a major barrier to both the treatment of Toxoplasma and its use in delivery of heterologous antigens and protein-based therapeutics," the authors conclude.
Finally, investigators at Icahn School of Medicine at Mount Sinai and elsewhere explore genetic contributors to autism spectrum disorder (ASD) using exome sequencing. The team narrowed in on 102 ASD-related genes by sequencing protein-coding portions of the genome in nearly 12,000 individuals with ASD and more than 23,500 unaffected controls. By bringing in additional gene function and tissue-based expression clues, the authors saw an over-representation of ASD-related genes from severe neurodevelopment and other pathways, along with genes known for increased expression at various stages of development in different human brain regions. "In cells from the human cortex, expression of risk genes is enriched in excitatory and inhibitory neuronal lineages, consistent with multiple paths to an excitatory/inhibitory imbalance underlying ASD," they write. GenomeWeb has more on the study, here