Mouth with probably over 240 species of bacteria inside
http://www.flickr.com/photos/mbaruzza_2/

It’s been an interesting week in the stratosphere with a fireball in Wisconsin caught on video and a giant ash plume from the eruption of Iceland’s Eyjafjallajökull volcano.

But I’m feeling a bit introspective. Published in The ISME Journal, researchers (including a couple from the J. Craig Venter Institute in Rockville and the Institute For Genome Sciences at the University of Maryland School of Medicine) finally determined the bacterial diversity of our mouths or at least of 10 lucky individuals.

The researchers collected 26 separate samples from different parts of each healthy person’s mouth and pooled them, collecting and amplifying the RNA sequences present. RNA (or ribonucleic acid) contains the important coding information from DNA. RNA is necessary to every living organism, transcribed from DNA and translated into protein. Without RNA, there would just be pieces of DNA code, unable to be read or to be used as a template to construct protein. By isolating and amplifying a specific piece of RNA present only in bacteria, scientists are able to determine specific species through deciphering the sequences. In this study, around 1000 sequences per mouth were analyzed.

So what did they find? Contrary to past estimates that the mouth harbors 500-700 different bacterial species, this study found about 240 belonging to 9 different phyla or groups. As you may expect, not every mouth is the same. Subject 4 had the greatest number of bacteria (lucky duck), and only around 50 different species were expected to be shared between any two individuals with 11 shared between all 10 of the people studied. If you’re really into species (and who isn’t?), the magic 11 are: Haemophilus parainfluenzae, Streptococcus oralis, Streptococcus sanguinis, Granulicatella adiacens, Veillonella parvula, Veillonella dispar, Rothia aeria, Actinomyces naeslundii, Actinomyces odontolyticus, Prevotella melaninogenica and Capnocytophaga gingivalis. Interestingly, although every subject had sequences belonging to the group of bacteria known as Neisseria, no single specific Neisseria species was shared across all subjects. Our mouth bacterial flora also appears to be very distinct from that found in our colon, confirming that these are very different environments (as if we didn’t know that already).

It’s already known that bacterial flora can be passed from mother to child. I wonder if this study had been conducted with healthy couples who kiss frequently, if they would find a more similar bacterial diversity than 10 strangers. But that study probably isn’t a strong candidate for NIH funding.

Stuttering is found in all cultures and languages, affecting 5% of children in twice as many boys as girls. Nearly 80% of childhood stuttering resolves itself, mostly in girls, leaving male stutterers outnumbering female stutterers 4:1. 60 million people in the world are stutterers, and Winston Churchill, John Updike, King George VI and James Earl Jones join their ranks. The history of stuttering is fraught with erroneous theories and damaging medical practices. The ancient Greeks thought that stuttering resulted from tongue dryness and recommended enlargement of the veins by surgical or chemical means. In the 1800s, stuttering was thought to be an anatomical defect, and surgical treatments were popular. By the 1900s, stuttering was ruled a psychological disorder and treated with conditioning and psychoanalysis that were eventually proven ineffective. The modern theory is that stutterers have a neurophysical problem that disrupts the precise timing in speech.

Human chromosomes; NIH

The evidence for a genetic component to stuttering is apparent, such as the existence of identical twin stutterers and a high incidence of stuttering in first degree relatives. Approximately half of stutterers have a family history of the disorder. By examining genetic linkage in families of stutterers, geneticists have honed in on several chromosomes that may be involved in stuttering.

In Kang and Drayna’s most recent study, they’ve focused on chromosome 12 to examine the genes involved in stuttering in the largest well-studied group of stutterers, a Pakastani family simply known as PKST72. By comparing the DNA of stutterers in the family to non-stuttering control subjects, the researchers were able to pinpoint the genetic sequences affected in stuttering individuals. Interestingly, the genes they identified affect the cell’s recycling center, the lysosome. The lysosome takes unwanted material in the cell, such as old proteins, and breaks them down into something more usable. In this family of stutterers, the genes that direct proteins to the lysosome for recycling are mutated, most likely resulting in a build-up of this cell litter in other compartments of the cell. Somehow this accumulation of trash in cells leads to speech disturbance. The way this occurs is unknown, and the implication of these results for both treatment of stuttering and future studies is profound.

One other thing of note is that all but two of the stutterers with these mutations were heterozygous, meaning that the mutations were only found on one of the two strands of chromosome 12. If the mutations were found on both strands of DNA, the affected persons may have had a severe lysosomal storage disease called mucolipidosis.

DNA is amazing.