All we need now is evidence of Mothra

Researchers have uncovered evidence of a giant sea scorpion; a fossilized claw that is so large, the creature that it belonged to would’ve been 2 metres long–longer than humans are tall.  The fossil record has provided evidence of other super-sized bugs, but this new scorpion would be the biggest found to date. 

It’s believed it lived about 400 million years ago, along with other really large arachnids and insects; organisms that died out in an epic evolutionary struggle with armoured fish.  At least, that’s what the paleontologists say. 

The timing of this discovery is a bit coincidental for me, personally, as I have just finished reading Dan Brown’s Deception Point.  So, an article about giant sea bugs immediately caught my attention.  And if you don’t know what I’m talking about, here’s the first (and probably only) book recommendation to appear on this blog:  Read Deception Point by Dan Brown, it’s good.

I hope John Tory reads this

It seems our understanding about how evolution can occur is changing.  Work published in the prestigious Proceedings of the National Academy of the Sciences (PNAS, tee-hee) has found evidence of sympatric speciation; the separation of a population into different species without the need of a physical, geographic barrier.  

The researchers, led by Canadian scientists at Queen’s University, have found that within five colonies of tropical birds living in the archipelagos where there are two populations with distinct breeding seasons, there is significant genetic variation between the populations and, in two of the colonies they have stopped exchanging genes entirely.  The data the researchers collected indicates at least four of these populations have arisen simply out of the difference in breeding periods. 

Darwin had initially proposed that sympatric speciation could occur, and now here’s the evidence.  Researcher Andrea Smith said “that it’s challenging the idea that you need a geographic barrier for species to arrive.”

It’s a good example of how a scientific theory, such as evolution, can be refined when new evidence is found.   

Highlight Reel

No one story has been sufficient inspiration for me to dedicate to it an entire post, however there were a few interesting stories I noticed recently.

In a recent post I mentioned how researchers are looking into clays used as ancient remedies for potential treatments of drug-resistant bacteria.  Well, this recent health alert in Ontario suggesting physicians be on the look-out for a particular sub-strain of Streptococcus pneumoniae 19A provides an example of why this work could be very valuable.  These bacteria commonly cause ear, chest and throat infections which can be readily treated with antibiotics, however this newly identified sub-strain cannot. 

In another post, I discussed research into pheromones, where attraction is (at least, partially) controlled by the sense of smell.  Well, here’s more evidence odours can have a direct affect on behaviour.  Japanese researchers have found a smell receptor in mice that detects the odour of cats and causes the mice to run away, naturally.  It was found that mice who had this receptor turned off would not fear cats, and in fact, they would play with kittens.  To demonstrate the importance of this particular receptor, mice were engineered to have a very poor sense of smell.  While these mice had difficulty detecting the odour of cats, once they did, their response was to flee.  The researchers say this points out there are two distinct functional modules of the olfactory system, one for innate responses to odours and one for learned, associative responses.

Finally, in February of this year researchers investigating if there’s a genetic factor behind type II diabetes stumbled upon a gene called FTO that is related to obesity.  However, at the time that’s all they could say–if you have two copies of a particular variant of the FTO-gene you were on average 3 kg heavier.  The challenge was then to find out how this gene worked and there have been a couple of recent discoveries working towards this end. 

In research involving mice, it has been found that the protein this gene codes for, the FTO-protein, would accumulate in the hypothalamus in the brain.  However, up to 60% less of this protein was found in the hypothalamus’ of mice who were underfed when compared to mice on a regular feeding schedule, suggesting the function of the gene may be related to appetite. 

In separate work, scientists examined the structure of the FTO-protein finding it is very similar to other known DNA demethylase enzymes; enzymes that repair altered DNA by removing a chemical moiety known as a methyl group.  The question of how demethylating DNA plays a role in obesity is still open, but it’s a crucial first step in determining how this gene and its related protein function.

While I am interested in how this gene actually works, I’m just glad there’s another reason why I can claim I’m at least 3 kg heavier than I should be, aside from the amount of time I spend sitting on my butt in front of a computer doing things like writing on my blog.