The mechanism that controls the internal 24-hour clock of all forms of life from human cells to algae has been identified by scientists.
Not only does the research provide important insight into health-related problems linked to individuals with disrupted clocks – such as pilots and shift workers – it also indicates that the 24-hour circadian clock found in human cells is the same as that found in algae and dates back millions of years to early life on Earth.
As I have argued before, one key to the success of bacteria-as-terraformers is their ability, as single-celled organisms, to network with each other both physiologically and genetically. Well, recent evidence strongly suggests that such connections also include charitable behavior, where certain cells come to the aid of their neighbors:
Humans are capable of great charity, taking hits to their bank accounts and bodies to benefit their peers. But such acts of altruism aren’t limited to us; they can be found in the simple colonies of bacteria too.
Bacteria are famed for their ability to adapt to our toughest antibiotics. But resistance doesn’t spring up evenly across an entire colony. A new study suggests that a small cadre of hero bacteria are responsible for saving their peers. By shouldering the burden of resistance at a personal cost, these charitable cells ensure that the entire colony survives.
Read the rest about this eye-popping study here.
Jonah Lehrer has some more thoughts on the Decline Effect:
The first letter, like many of the e-mails, tweets, and comments I’ve received directly, argues that the decline effect is ultimately a minor worry, since “in the long run, science prevails over human bias.”
Lehrer then quotes Feynman who discusses the famous 1909 oil-drop experiment and explains why it took so long for scientists to zero on the correct measure for the charge of the electron:
Why didn’t they discover that the new number was higher right away? It’s a thing that scientists are ashamed of—this history—because it’s apparent that people did things like this: When they got a number that was too high above Millikan’s, they thought something must be wrong—and they would look for and find a reason why something might be wrong. When they got a number closer to Millikan’s value they didn’t look so hard.
As Lehrer notes, this is yet another example of the “selective reporting in science.” But Feynmann was trying to make another point:
he warned the Caltech undergrads to be rigorous scientists, because their lack of rigor would be quickly exposed by the scientific process. “Other experimenters will repeat your experiment and find out whether you were wrong or right,” Feynman said. “Nature’s phenomena will agree or they’ll disagree with your theory.”
But Lehrer is quick to puncture the obvious naivety associated with this claim:
It the previous posting, we saw there was good reason to think mitochondria were a necessary prerequisite for the evolutionary emergence of metazoan-type complexity. Again, as Lane and Martin clearly point out:
Our considerations reveal why the exploration of protein sequence space en route to eukaryotic complexity required mitochondria. Without mitochondria, prokaryotes—even giant polyploids—cannot pay the energetic price of complexity; the lack of true intermediates in the prokaryote-to-eukaryote transition has a bioenergetic cause.
So we can see that natural selection, functioning as a designer-mimic, is, like other designers, constrained (and thus guided) by the materials used to express the design. Just as there is no reason to think natural selection could craft something as complex and sophisticated as the prokaryotic cell without proteins, natural selection apparently cannot craft something as complex as a mouse or squid without the eukaryotic cell plan. That’s why cells had to be first re-tooled through an endosymbiotic relation.
But why haven’t bacteria, after billions of years, ever been able to discover a method of evolving something mitochondrial-like without relying on endosymbiosis? At first, it might seem to be simply an issue of scale, as the typical mitochondrion is roughly the same size as the typical bacteria. But there are bacteria that are as large as some eukaryotic cells and it looks like they try to mimic mitochondria, but never quite make it. One such bacterium is Thiomargarita.
Lane and Martin discuss this bacterium and Myers summarizes their argument as follows:
