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Zzzz

clock.jpgI wrote an article about sleep and this weekend’s time change for a local student newspaper. Initially I really wanted to write about the molecular mechanisms behind it, but it was too complicated and long, so eventually it ended up being really quite general. I still wanted to share the cool molecular background, so I’m putting up some of the deleted sections here. You can read them on their own out of context, but you’ll need the first one to understand the second one.

The final article is here. You might need to register, but it’s free.

One of the middle versions of the article, before I kicked out all the genetics, contained this paragraph:

The circadian genes were first identified in fruit flies, but were later found to be quite similar in mammals. In the mammalian biological clock transcription of a group of Period (Per) and Cryptochrome (Cry) genes is activated by a complex of the proteins CLOCK and BMAL1. Once the PER and CRY proteins are expressed, they form a complex with a third protein, Casein Kinase I. This PER/CRY/CKI complex binds to the CLOCK/BMAL1 complex and inhibits it. Now that CLOCK/BMAL1 can no longer activate transcription of Per and Cry, their levels will go down. Eventually this big complex falls apart, and CLOCK/BMAL1 will activate transcription of Per and Cry again, starting a new cycle.

And the initial version that my writing group read had this section, which is my absolute favourite part of the whole thing, but was just way too specific, and I threw it out myself even before sending it out to the editor:

Not everyone has the same body clock. At the extreme end of the spectrum there is the case of a Utah family that goes to bed at 7.30 PM and gets up around 4 AM every day. You’d think they could just practice staying up later and get used to more normal hours, but the problem is genetic. They have Familial Advanced Sleep Phase Syndrome (FASPS), which means their inner clocks are just not quite right. They have a mutation in the Per2 gene that disrupts the circadian cycle.
Normally, the protein Casein Kinase I helps synchronize the complexes it forms with PER and CRY by phosphorylating them. Phosphorylation is a common posttranslational modification of many proteins. It’s the addition of a phosphate group to certain amino acids in a protein that changes the activity of the protein: it makes it interact differently with its neighbour proteins and either inhibits or activates them. Only the amino acids serine, threonine, and tyrosinase can be phosphorylated this way. In the Utah family with the strange bedtime hours, there is one single mutation in the Per2 gene that changes a serine in the PER2 protein to a glycine. The glycine amino acid can’t be phosphorylated by casein kinase I, and this small mistake causes their entire body clocks to be out of synch.

(The references for this last section are under the cut below.)

So, this is how much editing occured to get to the final sleep piece. I miss the genetics, but it’s much more readable now. Admit it, who actuallly read the last blockquote? If that doesn’t put you to sleep…. ;)

FASPS references:
C.R. Jones et al. (1999), “Familial Advanced Sleep Phase Syndrome : A short-period circadian rhythm variant in humans”, Nature Medicine, 5(9), 1062-1065
Kong L. Toh et al. (2001), “An hPer2 Phosphorylation Site Mutation in Familial Advanced Sleep Phase Syndrome”, Science 291 (5506), 1040-1043

1 comment to Zzzz

  • I read the second blockquote but not the first. Capital letters bore me, but add some protein phosphorylation and functional outputs and I’m yours.