Category: Evolution (page 4 of 4)

using HIV to fight cancer

A model of HIV.

HIV, like other viruses, mutates rapidly in response to changes in its environment. This ability to rapidly change gives them the ability to evade the natural defense mechanisms our bodies trigger once we are infected. Researchers have found a way to exploit this property of HIV to generate proteins that will help fight cancer. From Popular Science:

As HIV replicates, it creates slightly new versions of itself over successive generations – this allows it to readily resist most of the drug cocktails and anti-viral treatments developed to fight it. But it could also allow HIV to serve as a sort of molecule factory, creating new iterations of compounds that work in slightly different ways.

The CNRS team modified the genome of HIV by inserting a human gene for a protein called deoxycytidine kinase (dCK). This protein is found in all cells and is important for activating anti-cancer drugs. Researchers would like to make a more potent form of dCK that would allow cancer drugs to work more effectively, which could in turn require less of them, causing fewer side effects and less toxicity.

The team multiplied this mutant HIV through several generations, yielding an entire library of mutant dCK proteins, about 80 in all. Ultimately, they found a variant that induces tumor cells to die. With just 1/300th the dose of cancer-killing drugs, this one-two protein punch is just as effective at stopping tumor growth.

For more read here. For the original research paper from PLoS Genetics go here.

DNA, RNA, XNA

A DNA helix

DNA & RNA genetic information to be stored and propagated through the generations. Now researchers have created new molecules called XNAs by replacing the sugar molecules on the DNA or RNA phosphate backbone with an analog. From Science News:

The researchers, led by Philipp Holliger of the MRC Laboratory of Molecular Biology in Cambridge, England, did make completely new genetic molecules. In the backbone of every DNA molecule there are repeating units of deoxyribose sugar, in the RNA backbone it’s ribose sugar. Instead of those sugars, the various XNAs have different molecules in their backbones: a five-carbon sugar called arabinose in ANA, the ringed structure anhydrohexitol in HNA, and threose, a four-carbon sugar in TNA. The scientists also created XNA molecules called FANA (2´-fluoroarabinose), CeNA (cyclohexene) and LNA (“locked” ribose analog).

In a second bioengineering feat, the researchers created special enzymes for the XNAs so that they could evolve. This requires enzymes that can “read” the order of molecular components in a strand of XNA and use that information to build a complementary strand of DNA. Working with an enzyme from a sulfur-loving microbe, the team selected for versions that could “read” each of the XNAs. The researchers also made enzymes that could do the reverse: read DNA and use that information to build XNA.

Because the XNAs can’t copy themselves without help from DNA, it’s not truly synthetic life, says Joyce. But the molecules do undergo good old-fashioned evolution. With HNA, for example, the researchers created a random population of HNA molecules, then exposed them to a bunch of target molecules (such as proteins or RNA) for the HNA to attach to. Most of the HNAs didn’t do diddly-squat, but a fraction were slightly better at connecting to the target molecules.

More here and here.

does an all meat diet lead to loss of sweet-tooth?

Maybe:

A gene crucial for detecting sweet taste carries disabling glitches in seven of 12 mammals analyzed in a new study. The sweet-blind animals are spotted hyenas, Asiatic small-clawed otters, two catlike wild hunters (fossa and banded linsang), sea lions and two kinds of seals — all predators.

But then again, maybe not:

This loss isn’t universal among dedicated meat eaters, though. Red wolves, Canadian otters and aardwolves (hyena relatives that stalk termites) turn out not to have lost their genetic sweet spot.

…[And] from the opposite point of view, some animals that don’t specialize in meat nevertheless may have lost their ability to taste sweetness. For instance, chickens, which eat both plant and animal foods, don’t seem to notice sweetness in their food and appear to lack the functional sweet gene, says Peihua Jiang, also of Monell and a coauthor of the new study.

Chickens are just one reason that Huabin Zhao of Wuhan University in China isn’t convinced by the meat-eater/sweet-loss scenario. He has found sweet loss among vampire bats, which are blood feeders. Narrow diet specialization might be a better explanation, he suggests.

From ScienceNews

Further Reading: [PNAS] abstract available

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