A common hospital superbug called Clostridium has a protective coat of armor that can self assemble when put into a test tube on its own, which may have important commercial uses in nanotechnology, according to scientists.

Like many other micro-organisms, Clostridium difficile produces a lattice coat made of proteins to surround its cell wall and protect it like a suit of armour. The complete protein coat is then attached to the underlying cell wall with chemical bonds.

“We have discovered that these protein coats have a remarkable ability to self-assemble when they are taken off the bacteria and put into a test tube.

How we come to express the genes of one parent over the other is now better understood through studying the platypus and marsupial wallaby – and it doesn’t seem to have originated in association with sex chromosomes.

New research published in BMC Evolutionary Biology has shed light on the evolution of genomic imprinting, in which specific genes on chromosomes that have been inherited from one parent are expressed in an organism, while the same genes on the chromosome inherited from the other parent are repressed.

Imprinting arises from some kind of ‘epigenetic memory’ – modifications to the DNA from one parent, such as the way the chromosomal material is packaged, that do not allow particular genes to be expressed. The reasons why imprinting evolved are not understood.

Bacteria that thrive in oxygen starved environments have been used successfully to target cancer tumors, delivering gene therapy based anti-cancer treatments, according to scientists.

For about half of cancer sufferers traditional treatments such as radiotherapy and chemotherapy are ineffective, so alternative techniques are being developed to target their tumors.

“To target a tumour with gene therapy you need three things. You need to be able to distinguish the tumour from its surrounding healthy tissue. You need to identify a therapeutic gene which will treat the problem. And you need some way of delivering the gene to the tumour”, says Dr Jan Theys of Maastricht University, the Netherlands.

So vital is the p53 tumor suppressor gene in controlling cancer that its dysfunction is linked to more than half of human cancers. At the same time, the gene’s capacity for shutting down cell growth, even causing cells to commit suicide if necessary, is so absolute that it must be tightly regulated to maintain the optimal balance between protecting against cancer and permitting normal growth.

Now, a study by scientists at The Wistar Institute reveals new levels of subtlety in the body’s management of this all-important tumor suppressor gene and the protein it produces.

With the help of genetically engineered mice whose livers turned into glowing light bulbs, researchers at the Salk Institute for Biological Studies have illuminated the underpinnings of an insidious and growing health concern— type II diabetes.

In the study published in the September 5 advanced online edition of Nature, the researchers report that a protein called TORC2 serves as a key biochemical control point linking feeding, insulin, and elevated blood sugar production in the liver.

According to new research, two key proteins join together at the precise location where energy of motion is turned into electrical impulses. These proteins, cadherin 23 and protocadherin 15, are part of a complex of proteins called “tip links” that are on hair cells in the inner ear. The tip link is believed to have a central function in the conversion of physical cues into electrochemical signals.

“Mutations in [the genes] cadherin 23 and protocadherin 15 can cause deafness as well as Usher syndrome, the leading cause of deaf-blindness in humans,” says Professor Ulrich Mueller, of the Scripps Research Department of Cell Biology and Institute for Childhood and Neglected Diseases.