Two years ago, the project of sequencing the Neanderthal genome started. They (Max Planck Institute & 454 Life sequencing) promised to end by this year. Well, they kept their promise. Frankly, some mitochondrial DNA sequences (mtDNA) have been published but contamination was the major defect in those published sequences. They collected more than 60 bone specimens from museums (We’re talking about 38,000-year-old bone); they repeated the sequencing for 35 times in the same clean room of extraction to avoid contamination with human DNA.

From the total 13 protein-encoding genes of the sequenced mtDNA, they identified only one with amino acids difference than the human sapien version. It is cytochrome c oxidase subunit 2 (COX2 – part of the respiratory chain), but even this difference has no significant effect on the functional domain of COX2. They hope to answer this questions in a few months: Why Neanderthals died out & human didn’t?!

We already know that Neanderthals & humans share 99.5% of the sequence, but answering questions about having a common ancestor & extinction through absorption (bred with humans) needs lots & lots of researches, collecting & sequencing samples at different time intervals to come with hypotheses. The mtDNA is not enough as Trinkaus (an expert on Neanderthal biology and human evolution) said: “The genome sequence data may tell us something about the selection of a couple of proteins, but it tells us nothing about language or social behavior.”

Image credits:
Reconstruction of a Neanderthal child from Gibraltar: http://en.wikipedia.org/
First complete Neanderthal genome sequenced: http://www.nature.com/

To be frank, I was really underestimating these bacteria. Streptococcus iniae, bacteria bothering fish, what’s the big deal? But when I read that it cause them meningoencephalitis due to systemic dissemination resulting in death, it made me sad. They’re fish, you know, they don’t deserve such destiny. (We can’t say that about eating them, right?) Back to scientific details, S. iniae was isolated from Amazon dolphins (Inia) but it has a very wide host range, it can infect fresh & saltwater species like salmon, yellowtail & hybrid striped bass (HSB). It also can infect immunocompromised as well as elders from humans.

S. iniae are beta-hemolytic streptococci, they have M protein (present in cell membrane) then the capsular polysaccharide which interfere with phagocytosis. They also have phosphoglucomutase which make their cell wall rigid & resistant to peptide antimicrobials, besides their streptolysin S. I’ve to tell you this, this iniae is a walking disaster, just like the human version S. pyogenes.

So what scientists tell us this time? Thanks to 454 pyrosequencing & bioinformatics, they identified extra virulence factors of S. iniae. Regulations in S. iniae are done through a Mga-like Mgx loci (multiple gene regulator of group A streptococci). It regulates the virulence factors. It’s used to be known that M-protein is a component of that Mga. This time, discovery of extra components takes place, the M-like surface protein (simA) & C5a peptidase (scpI). A word about scpI, its role is to inactivate C5a (the complement component) to hinder the complement reaction & also has a role in adhesion to epithelial cells.

Actually they’re looking forward to using the mutant delta-simA as a live attenuated vaccine against S. iniae. (Vaccine for fish?) They made mutations in both C5a-like peptidase & simA, apparently simA had the leading role in the virulence of the studied strain of S. iniae. So a new approach of vaccination will be developed instead of the old M protein vaccination strategy which requires multimeric vaccination (to provide protection against several serotypes) & showes autoimmune response. Unlike the ordinary M protein vaccination, vaccination with the mutant delta-simA will result in development of humoral as well as cell-mediated immunity.

Image credits:
Fish – Cartoon: http://www.robdoyle.co.uk/