Cell biology

A week ago, VJT put up a useful set of excerpts from Axe’s 2010 paper on proteins and barriers they pose to Darwinian, blind watchmaker thesis evolution. During onward discussions, it proved useful to focus on some excerpts where Axe spoke to some numerical considerations and the linked idea of islands of specific function deeply isolated in AA sequence and protein fold domain space, though he did not use those exact terms. I think it worth the while to headline the clips, for reference (instead of leaving them deep in a discussion thread): _________________ ABSTRACT: >> Four decades ago, several scientists suggested that the impossibility of any evolutionary process sampling anything but a miniscule fraction of the possible protein sequences Read More ›

. . . and blatant denial is not an appropriate response to the reality of and/or easily known facts concerning functionally specific complex organisation and /or associated information, FSCO/I: Facts are stubborn things, but people can be more stubborn than that. (That is, there are two types of ignorance, I: simple ignorance because one does not know the facts and/or may not understand them, but also II: ideological closed-mindedness due to being controlled by mind-closing agendas hostile to, selectively hyperskeptical towards and dismissive or suppressive of inconvenient facts, . . . such as those we just saw regarding FSCO/I.) Why am I saying this? Poster-boy no 1, rich @ 252  in the UD no bomb thread: [KF:] “Your comment no Read More ›

Mutations are used to explain evolution but also cause cancer. Biologists have discovered conditions for multiple mutations. Can we therefore infer that evolution via mutations is more likely? or that enhanced mutations will cause faster species degradation and extinction?

Biologists describe mechanism promoting multiple DNA mutations

DNA mutations—long known to fuel cancer as well as evolutionary changes in a living organism—had been thought to be rare events that occur randomly throughout the genome.

However, recent studies have shown that cancer development frequently involves the formation of multiple mutations that arise simultaneously and in close proximity to each other. . . .Anna Malkova, associate professor of biology in the UI College of Liberal Arts and Sciences, notes that the DNA repair pathway, known as break-induced replication (BIR), can promote clusters of DNA mutations.

“Previously, we have shown that double-strand DNA breaks, which can result from oxidation, ionizing radiation and replication errors, can be repaired by BIR,” says Malkova.

“During BIR, one broken DNA end is paired with an identical DNA sequence on another chromosome and initiates an unusual type of replication, which proceeds as a migrating bubble and is associated with the accumulation of large amounts of single-strand DNA,” she says.

In the Cell Reports study, researchers subjected yeast cells undergoing BIR to alkylating (cancer cell-killing agents) damage. “We found that the single-stranded DNA regions that accumulate during BIR are susceptible to damage that leads to the formation of mutation clusters,” explains Cynthia Sakofsky, postdoctoral fellow at the UI and one of two co-first authors on the paper. “These clusters are similar to those found in human cancer,” she says.

Importantly, say the researchers, the paper provides a mechanism to potentially explain how genetic changes form in human cancers. Thus, it will be critical for future research to determine whether BIR can form clustered mutations that lead to cancer in humans.

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Are you what you eat? Or what’s eating you?
Novel virus discovered in half the world’s population

A new study led by researchers at San Diego State University has found that more than half the world’s population is host to a newly described virus, named crAssphage, which infects one of the most common types of gut bacteria, Bacteroidetes. This phylum of bacteria is thought to be connected with obesity, diabetes and other gut-related diseases. . . .It’s unknown how the virus is transmitted, but the fact that it was not found in very young infants’ fecal samples suggests that it is not passed along maternally, but acquired during childhood. The makeup of the viral DNA suggests that it’s circular in structure. Further laboratory work has confirmed that the viral DNA is a singular entity, but it’s proven difficult to isolate. . . .
Some of the proteins in crAssphage’s DNA are similar to those found in other well-described viruses. That allowed Edwards’ team to determine that their novel virus is one known as a bacteriophage, which infects and replicates inside bacteria—and using innovative bioinformatic techniques, they predicted that this particular bacteriophage proliferates by infecting a common phylum of gut bacteria known as Bacteriodetes.
Gut punch
Bacteriodetes bacteria live toward the end of the intestinal tract, and they are suspected to play a major role in the link between gut bacteria and obesity. What role crAssphage plays in this process will be a target of future research.. . .

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