Welcome to your weekly dose of cell and molecular biology. As always, I’ll choose select posts from blogs that I read – please do contact me with specific posts that you’d like “Cells Weekly” to link to, or topical blog discussions that I might be missing. And of course, please link to the “Cells Weekly” to share it with others.
- Biosingularity: Regulating the nuclear architecture of the cell
- The Tree of Life: Classic papers in genetics and evolution that are available in Pubmed Central – Paper 1 – Luria and Delbruck on the origin of mutations
- The Daily Transcript: Different types of signal sequences?
- Gene Expression: PSD95-Spines
- Omni Brain: Transcription factors made easy
- Pure Pedantry: Presynaptic vesicles are hemifused
- The Mouse Trap: History in the making – the neurogeneisis discovery
In the wake of the Australian Senate’s decision to pass the human embryo cloning legislation, another Australian research breakthrough is likely to strengthen the case for embryonic stem cell research.
University of New South Wales (UNSW) academics have proven that tumours can be prevented from forming when embryonic stem cells are transplanted.
“Whilst embryonic stem cells have great potential to deliver therapies for disorders, such as diabetes, a fear has been that they will form tumours because of the presence of undifferentiated cells,” said UNSW Professor Bernie Tuch of the Diabetes Transplant Unit, who led the team responsible for the discovery.
Living things are resourceful, which is a comforting thought unless the living thing in question is a pathogen or a cancer cell. Noxious cells excel at developing drug resistance, outwitting immune systems, and evading cellular controls. They even show an unhealthy talent for surviving internal perturbations such as mutations that affect the function of vital genes, and they do this by evolving new mechanisms to perform old tasks. Somehow the bad guys find a workaround.
That observation led Norman Pavelka, Giulia Rancati, and Rong Li, researchers at the Stowers Institute for Medical Research in Kansas City, MO, to step back and consider the basic process by which cells adapt to the loss of seemingly irreplaceable genes. The researchers reasoned that understanding how cells adapt to internal perturbations could offer insight into how pathogens and cancer cells mutate to evade the body’s defenses and resist treatment with drugs.
Science may be one step closer to understanding how a limb can be grown or a spinal cord can be repaired. Scientists at The Forsyth Institute have discovered that some cells have to die for regeneration to occur. This research may provide insight into mechanisms necessary for therapeutic regeneration in humans, potentially addressing tissues that are lost, damaged or non- functional as a result of genetic syndromes, birth defects, cancer, degenerative diseases, accidents, aging and organ failure. Through studies of the frog (Xenopus) tadpole, the Forsyth team examined the cellular underpinnings of regeneration.
The Xenopus tadpole is an ideal model for studying regeneration because it is able to re-grow a fully functioning tail and all of its components, including muscle, vasculature, skin, and spinal cord. The Forsyth scientists studied the role that apoptosis, a process of programmed cell death in multi-cellular organisms, plays in regeneration. The research team, led by Michael Levin, Ph.D., Director of the Forsyth Center for Regenerative and Developmental Biology, found that apoptosis has a novel role in development and a critical role in regeneration. According to Dr. Levin, “Simply put, some cells have to die for regeneration to happen.”
Nothing in the cellular world is flat. Even the flattest of basement membranes has topography; bumps, if you like, beneath the cellular mattress.
Unlike the princess kept awake by the pea, human embryonic stem (HES) cells do better when cultured on a substrate deliberately printed with nanoscale grooves and ridges, according to researchers from the University of Wisconsin–Madison.