Science continues to uncover fascinating features of our biotic reality. In one study, we again see the crucial role of gene duplication in the evolution of humans:

“After surveying gene families that are common to both humans and chimps, we observed in the human genome a significant increase in the duplication of various genes, including some that influence brain functions. This may provide new information about what it means to be human,” says Nello Cristianini, Professor of Artificial Intelligence at Bristol University, who statistically analysed the data with specially created software tools. The results support mounting evidence that the simple duplication and loss of genes has played a bigger role in our evolution than changes within single genes…..humans have gained 689 genes (through the duplication of existing genes) and lost 86 genes since diverging from their most recent common ancestor with chimps. Including the 729 genes chimps appear to have lost since their divergence, the total gene differences between humans and chimps was estimated to be about 6 percent.

Here is a study that speaks for itself:

The oldest-known animal eggs and embryos, whose first pictures made the cover of Nature in 1998, were so small they looked like bugs – which, it now appears, they may have been. This week, a study in the same prestigious journal presents evidence for reinterpreting the 600 million-year-old fossils from the Precambrian era as giant bacteria.

I’ve written about extreme evolution before, and a new study suggests this might be very common:

Imagine her surprise, then, when research scientist Brett Baker discovered three new microbes living amidst the bacteria she thought she knew well. All three were so small - the size of large viruses - as to be virtually invisible under a microscope, and belonged to a totally new phylum of Archaea, microorganisms that have been around for billions of years.

Homeostasis is the essence of life. A molecular example is iron homeostasis, where a large protein, IRP1, not only has dual functions, but can serve as both sensor and effector in controlling iron concentration levels in the cell. A recent study shows that its ability to control gene expression is surprisingly sophisticated.

IRP1 is a very large protein, composed of about 900 amino acids arranged into four major domains.

“We expected that IRP1 would open up the two major domains facing each other along a hinge, rather like a clam shell, to accommodate the RNA binding,” Walden said. “What we didn’t expect was that that opening up would also involve extensive movement within the domains.”

The researchers also found two widely separated contact sites between IRP1 and the iron responsive element, said Karl Volz, associate professor in of microbiology and immunology at UIC and principle investigator of the study.
“This is one of the highest affinity bindings we have ever seen. The effect of binding a single iron responsive element, through interactions at two separate binding sites, essentially eliminates the possibility of non-specific binding,” Volz said.

Finally, silent mutations occur when a base-pair substitution does not result in an amino acid substitution. The conventional view is that such mutations are perfectly neutral, but a recent study indicates otherwise. It is suggested that such mutations “represent rare codons for which translation machinery is not optimized. The resulting interruption of the rate at which mRNAs are translated could affect how a protein is folded, they said.”