This is a fascinating area – methods for amplifying DNA from single cells for complete genome sequencing. The current approach uses isothermal multiple displacement amplification MDA, followed by 454 sequencing. Biotechnology is getting closer towards its origins, yea, yea.

Addendum

We can now add also single cell protein analysis – microfluidic devices that can dissolve and separate proteins before quantifying them by fluorescence in confocal microscopy. Several groups tried to increase the signal-noise ratio by decreasing capillary dimension (leading to clogging) while the new study widens the excitation laser.

The forthcoming SNP whole genome association studies will draw a lot of attention. I already have the problem of many interacting SNPs where I am suggesting to divide significant results in 3 compartments – local (LD effects), longrange (cis transcription factor effects) and pathway effects (gene family, system wide effects). The main problem are false positives that can even not be overcome by techniques like FDR. Yea, yea.

A nature genetics paper shows that a single mutation in Pseudomonas has pleiotropic effects – not limited to the level of proteins in the particular network but changing also their relationships. Sounds like a soccer match where a player has to leave  the court – which changes positions of all remaining players. “The adaptive mutation draws proteins into tighter coregulation”, yea, yea.

The French department Finestière of Brittany is the named end of world and always nicely illuminated by impressive phares. Where is the end of the submicron world – at GFP labelled proteins?

-moblog- HMG has an interesting paper of Fei Sun and Renee H. Martin – showing a first visable recombination map of the male human genome. They obtained testicular samples from 10 males where each contributed 100 pachytene-stage cells. Chromosomes were identified by blue CREST centromere coloring and yellow MHL1 coloring of crossing over sites. Unfortunately the paper is not so easy to read but they have excellent figures. On average there are 50 cross-overs per set (which is more than I expected). The total number goes down from 52 at age 30y to 46 at age 80y (which may explain the higher chance of aneuploidy at a higher age). Individual crossover frequencies look extremely variable, chromosomal locations are clustering at different site -see my recent blog on recombinogenic sequences. Activity at centromeres was always low while chromosome 21q showed a high individual variablity. Why was there never detailed workup of physical and linkage map? Nay, nay.