In the tragic Huntsville shootings reported in Nature News Feature (Life after Death. http://www.nature.com/news/2010/100512/full/465150a.html. Nature 465, 150-155; 2010), Amy Bishop, an Assistant Professor in the University of Alabama’s biology department, methodically shot her colleagues during a departmental meeting, killing three and seriously injury three others.

Long after the shots rang out during that fateful departmental meeting, the ordeal still continues to haunt the victim’s families as well as students and trainees in the now shattered department. While colleagues pitch in to bring the department back to life, one could not help but ask why this horrible crime was committed. Why would an assistant professor do the unthinkable?

Researchers have come a long way from initially cracking the DNA code since the time of Watson and Crick, to now unveiling the complex layers of molecular codes that make up the cell’s molecular fingerprint.

These codes are no longer restricted to the 4 nucleotide codes of the DNA sequence, but rather a complex web of coding systems that regulate every stage of gene expression, including the epigenetic codes (transcriptional), microRNA codes (translational), as well as codes derived from alternative splicing of RNA transcripts (post-translational). While the existence of these codes are now dogma to most cell biologists, precisely how these codes dictate the identity of cells in a multicellular organism still remains elusive.

Mental retardation in autism is known to arise from a plethora of rare de novo mutations of key protein components in the synapse- the basic neuronal connection in the brain’s hardware. In a recent study published in Nature Genetics, Berkel and colleagues identified yet another de novo mutation associated with autism, which essentially consist of a series of loss of function mutations of the protein Shank2- a member of the postsynaptic scaffolding proteins located in the receiving end of synaptic connections known as the post-synaptic terminal (Berkel et al., 2010).

Since the rediscovery of the cancer stem cell hypothesis by Peter Dirks at the University of Toronto, researchers often use these cancer stem cells (or cancer initiating cells) as the scapegoat to explain why cancers are so hard to treat.

Multiple sclerosis (MS) is a devastating autoimmune disease, where the immune system attacks the white matter throughout the nervous system. While the cause for MS is currently unknown, epidemiological data so far suggests that the disease is likely triggered by both environmental and genetic factors. To pinpoint the molecular mechanism for MS, Sergio Baranzini and colleagues at UCSF conducted a recent twin study on multiple sclerosis using advanced tools such as genomic deep sequencing analysis. In their study published recently in Nature, Baranzini analyzed immune cells from identical twins where one of the twins has developed MS (Barazini et al., 2010). Much to their surprise, the study found no significant genomic differences between the twins.

Neural stem cells have long been defined as origin of nervous system development, spontaneously giving rise to the heterogeneous multitude of cells that make up the brain. Remarkably, neural stem cells seem to have the uncanny sense to differentiate at the right time and place, and to the appropriate fate, to produce a complex network consisting of neuronal connections and supportive glial cells.