Problem Solver
Amber Jolly
Areas Amber Jolly is Knowledgeable in:
Ocular infections by opportunistic pathogens, Intracellular Trafficking, Enzymology, Microbiology and Innate Immunity, Optics, Digital Pathology, Host-Pathogen Interactions, Microscopy, Image Analysis, Pathology, Cytoskeletal Biology, Biochemistry, Molecular Biology, Cell Culture, Cell Biology, Mouse Work, Neurodegenerative disease modeling (disease in a dish models for Alzheimer’s, Parkinson’s, ALS, Dementia, FTD and others), Cardiac disease modeling and Proarrythmia drug assessment for cardiotoxicity prediction applications.
Techniques Amber Jolly Uses:
Cell biology is my bread and butter, and my focus is always on molecular mechanisms. This means that my discoveries are usually a result of inductive reasoning, begin with a phenotype and employ a process of elimination to some degree to discover mechanism. However, I appreciate and can use both inductive and deductive reasoning.
Amber Jolly's Problem Solving Skills:
- Innate Immunity and infectious disease modeling
- Enzymology
- Molecular motor protein assays
- Biochemistry
- Digital Pathology
- Cell Biology
- Image Analysis
- Microscopy
- Modeling diseases of aging
- RNAi
- Molecular cloning
Amber Jolly's Problem Solving Experience:
- I created technical notes and webinars to teach customers how to create their own image analysis pipelines using CellProfiler software to analyze whole slide image scans of FFPE tissue slices.
- I discovered why ocular strains of Chlamydia trachomatis (Ct) cause scar tissue formation and blindness but urogenital strains do not cause blindness. I showed that urogenital strains, but not ocular strains, of Ct recruit monocytes to resolve the inflammatory response to Ct infection, which is initially mediated by conjunctival fibroblast cells.
- I demonstrated that the intact glycocalyx is critical to prevent infection in a healthy eye, and that inflammasome associated genes including IL-1R are actively modified during bacterial infection including Chlamydia trachomatis and Pseudomonas aeruginosa.
- I discovered how the genetic defect in individuals with cystic fibrosis causes enhanced intracellular survival and replication of Pseudomonas aeruginosa. This helps explain why people with cystic fibrosis succumb to Pseudomonas aeruginosa infection.
- I discovered a new cellular function of the kinesin-1 motor protein: mediating the sliding of interphase microtubules against one-another.
- I designed and implemented the first live cell genome-wide screen for intracellular motility regulation, using Drosophila melanogaster S2 cells treated with cytochalasin D to depolymerize the actin filaments.