Topic: CRISPR

Study genetic determinants of climate resilience in algae through the Golden Genome project supported by Revive and Restore. The work involves constructing insertional deletion libraries in microalgae, developing transformation approaches for the kelp Ecklonia radiata, and maintaining and cryopreserving algal cultures. The project combines molecular methods and CRISPR-based editing with marine climate-resilience research. This two-year, full-time appointment is based in Sydney. Salary: AUD 118,000–126,000 plus 17% superannuation and annual leave loading. Applications close on 5 November 2026.

H. Robert Horvitz's laboratory at MIT is recruiting a research technician to investigate molecular mechanisms of cell-fate determination and programmed cell death in Caenorhabditis elegans. The work includes genetic screens, CRISPR and transgenesis, molecular cloning, fluorescence microscopy, data analysis, animal husbandry, and general laboratory support in a highly integrative research environment.

Investigate resistance to KRAS inhibition across genetically distinct pancreatic cancers. The doctoral project studies tumour-cell and stromal mechanisms, including fibroblast effects, using organoid transplantation, mouse models, CRISPR, single-cell sequencing, flow cytometry and spatial methods. It seeks evidence for rational combination therapies and begins in October 2027.

UC Berkeley Molecular & Cell Biology seminar (Divisions of Biochemistry, Biophysics & Structural Biology; Cell Biology, Development & Physiology; and Genetics, Genomics, Evolution & Development) by Luke Gilbert of UCSF on repurposing CRISPR systems to activate and silence genes.

Jennifer Doudna discusses how CRISPR changed gene editing and what might come next. The conversation examines emerging applications, technical limitations and the ethical choices involved in altering genetic material, including how scientific progress can be paired with responsible use.

The field of human biology faces three major technological challenges. Firstly, the causation problem is difficult to address in humans compared to model animals. Secondly, the complexity problem arises due to the lack of a comprehensive cell atlas for the human body, despite its cellular composition. Lastly, the heterogeneity problem arises from significant variations in both genetic and environmental factors among individuals. To tackle these challenges, we have developed innovative approaches. These include 1) mammalian next-generation genetics, such as Triple CRISPR for knockout (KO) mic

Glioblastoma cells trigger pharmacoresistant seizures that may promote tumor growth and diminish the quality of remaining life. To define the relationship between growth of glial tumors and their neuronal microenvironment, and to identify genomic biomarkers and mechanisms that may point to better prognosis and treatment of drug resistant epilepsy in brain cancer, we are analyzing a new generation of genetically defined CRISPR/in utero electroporation inborn glioblastoma (GBM) tumor models engineered in mice. The molecular pathophysiology of glioblastoma cells and surrounding neurons and untra

Human genes associated with brain-related diseases are being discovered at an accelerating pace. A major challenge is an identification of the mechanisms through which these genes act, and of potential therapeutic strategies. To elucidate such mechanisms in human cells, we established a CRISPR-based platform for genetic screening in human iPSC-derived neurons, astrocytes and microglia. Our approach relies on CRISPR interference (CRISPRi) and CRISPR activation (CRISPRa), in which a catalytically dead version of the bacterial Cas9 protein recruits transcriptional repressors or activators, respec

The transcriptional co-activator Yes-associated protein-1 (YAP) and its paralog WW domain-containing transcription regulator 1 (WWTR1, TAZ) are known to regulate organ size, proliferation, and stem cell signaling in multiple tissue systems. However, their roles in nervous system development and neuronal differentiation have been understudied. Here, we set out to characterize YAP/TAZ expression changes and function in human neurogenesis in a cell lineage-specific and/or developmental stage-specific manner. To this end, YAP and TAZ knockouts were created in human embryonic stem cells using CRISP

Nicotinic acetylcholine receptors (nAChRs) are widely expressed throughout the brain and they are involved in the control of fundamental neural functions. One of the most common nAChR subtypes are heteromeric beta2-containing (beta2*) nAChRs. In the prefrontal cortex (PFC), beta2* nAChRs are expressed by different neuronal populations with different effects on behavior. To better understand functional role of beta2* nAChRs, we need to know which neuronal types in the PFC express them and what is the effect of these receptors on behavior. In the present project, we used FISH to map the expressi

Traditionally, research on AMPA receptors has predominantly focused on GluA1 and GluA2 subunits. However, emerging consensus now emphasizes the pivotal role of GluA3 in specific forms of plasticity and behaviors. Though, most of the research conducted thus far has employed complete knockout animal model of GluA3-encoding gene (GRIA3) where compensatory events during neurodevelopment may obscure GluA3’s function.To better dissect GluA3's contribution to complex behaviors, we employed two in vivo mouse models of GluA3 downregulation in adult mice. First, we chronically administered autoantibodie