In nominating John Pringle for the E.B. Wilson Medal, the ASCB's highest scientific honor, Daniel Lew, who is now at the Duke University Medical Center, described his friend and collaborator as the "father" of yeast cell biology. David Drubin, who introduced Pringle's Wilson lecture at the ASCB Annual Meeting last month in New Orleans, took it further. "Today it's hard to appreciate that back in the '70s and '80s, a lot of cell biologists didn't accept yeast as a eukaryotic cell," explained Drubin, a leading yeast cell biologist at the University of California, Berkeley.
Mathieu Coppey imagines using tiny magnets to move cells within living organisms. Coppey, a researcher at the Institut Curie in Paris, isn't envisioning a modern day version of "magnet therapy" touted a century ago by quack medical practitioners. Instead Coppey is using nanoparticle-size magnets to manipulate processes in cells.
Aside from Google Hangouts and Skype, it was the first time I'd been on video since my friend caught me singing to Spice Girls several years ago. I'd picked a high pressure venue for my return to video—the ASCB Annual Meeting in New Orleans. I was scheduled to give a short talk on Monday about scientists and social media. On Sunday though, I found myself in a small room in the convention center for a previously unscheduled coaching session on video with Susan Tomai, founder of Oratorio, a DC-based company offering media and presentation training.
Time-lapse movies of a cellular "heaven and hell," a dividing crane fly sperm cell undergoing, and the early development of muscle cells were recognized with the top three awards in the American Society for Cell Biology's Celldance "Really Useful" Cell Biology Video Contest for 2013. The special Public Outreach Award went to a group of cell biologists at the Dartmouth College, Geisel School of Medicine who danced their favorite cellular processes as The Cell Dance.
It may begin as a "simple" foot blister, but for patients with type 2 diabetes there is nothing simple about wounds that won't heal. That blister can evolve into a seriously infected wound that refuses to heal and, if gangrene develops, the patient's foot may have to be amputated. Such "simple" foot blisters and other diabetic ulcers or sores account for the vast majority of foot and leg amputations in the U.S. today. Paraplegics, quadriplegics, and anyone with severely limited mobility are also highly vulnerable to these chronic skin wounds as well as pressure ulcers and bedsores. Together, chronic wounds affect an estimated 6.5 million Americans at an annual cost of about $25 billion.
It seems an unlikely connection, and yet there is a significant link between Gaucher disease (GD), a purely genetic disease affecting lipid storage, and Parkinson's disease, a largely untreatable progressive degenerative movement disorder of the central nervous system that is often without a clear genetic cause. Those born with two recessive GD mutations, which cause a dangerous build-up of lipids, have a higher risk of developing Parkinson's disease than those with normal GD genes. More surprising is the higher risk for Parkinson's disease among carriers of GD mutation who have no overt GD symptoms, but still produce some level of the defective enzyme called glucocerebrosidase.
We talk about "hard wiring" the brain but our central nervous system is a work in progress. From the first neuron through childhood and adolescence, the neuronal network grows in complexity and size but also prunes out unneeded connections using molecules like the recently characterized enzyme, fidgetin, which makes strategic cuts in the microtubule scaffolding that holds up the cell's cytoskeleton and supports these connections. The ability of nerves to grow and prune diminishes as we mature until our adult neurons have mostly lost the power to reshape themselves.
A whimsically named fly gene, Sunday Driver, a.k.a. syd, and its mammalian analog, JIP3, seem to be in the driver's seat when it comes to parking the multiple nuclei of a skeletal muscle cell in their correct places, say researchers at the Sloan Kettering Institute (SKI). Getting that wrong and having mispositioned nuclei is a classic diagnostic sign of human congenital myopathies, a string of inherited muscle diseases such as Emery-Dreifuss muscular dystrophy (EDMD).