How do you keep different versions of Python on a Linux server?

Needed 2.7.2
This was what I did ...
wondering if there's a better solution.

http://www.python.org/download/releases/2.7.2/

• Gzipped source tar ball (2.7.2) (sig)
• Bzipped source tar ball (2.7.2) (sig)

untar
copy to ~/Python27

./configuremake make test

didn’t run make install (copies to the default dir?)


needed then to install a python library ..

Then run the setup.py script. For example, to install under your home directory:

$ export PYTHONPATH=$HOME/lib/python
$ python setup.py install --home=$HOME

This will install package the code up in a python egg that is installed in $HOME/lib/python, and install wrapper scripts for all the tools into $HOME/bin.


Reference
http://eli.thegreenplace.net/2011/10/10/installing-python-2-7-on-ubuntu/

heterozygous [PIC] funny!

credit Flow Cytometry

KIV scopeplusplus - SCOPE++: Sequence Classification Of homoPolymer Emissions - Google Project Hosting

SCOPE++ is a C++-based program for accurately identifying homopolymer in cDNA sequences using Hidden Markov Models. This can be extended to trimming poly(A)/poly(T) tails, or identifying A,C,G,T,or N homopolymer sequences.
http://code.google.com/p/scopeplusplus/

I love the 404 page at massgenomics...

hmmm trying to understand what's this about

OpenWetWare - Recent changes [en] - OSDDMalaria:OSDD Malaria Paper 1 - 1 hour ago

http://www.ncbi.nlm.nih.gov/pubmed/22482802

Am J Hum Genet. 2012 Apr 6;90(4):599-613.

Resolving the breakpoints of the 17q21.31 microdeletion syndrome with next-generation sequencing.

Itsara A, Vissers LE, Steinberg KM, Meyer KJ, Zody MC, Koolen DA, de Ligt J, Cuppen E, Baker C, Lee C, Graves TA, Wilson RK, Jenkins RB, Veltman JA,Eichler EE.

Source

Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA.

Abstract

Recurrent deletions have been associated with numerous diseases and genomic disorders. Few, however, have been resolved at the molecular level because their breakpoints often occur in highly copy-number-polymorphic duplicated sequences. We present an approach that uses a combination of somatic cell hybrids, array comparative genomic hybridization, and the specificity of next-generation sequencing to determine breakpoints that occur within segmental duplications. Applying our technique to the 17q21.31 microdeletion syndrome, we used genome sequencing to determine copy-number-variant breakpoints in three deletion-bearing individuals with molecular resolution. For two cases, we observed breakpoints consistent with nonallelic homologous recombination involving only H2 chromosomal haplotypes, as expected. Molecular resolution revealed that the breakpoints occurred at different locations within a 145 kbp segment of >99% identity and disrupt KANSL1 (previously known as KANSL1). In the remaining case, we found that unequal crossover occurred interchromosomally between the H1 and H2 haplotypes and that this event was mediated by a homologous sequence that was once again missing from the human reference. Interestingly, the breakpoints mapped preferentially to gaps in the current reference genome assembly, which we resolved in this study. Our method provides a strategy for the identification of breakpoints within complex regions of the genome harboring high-identity and copy-number-polymorphic segmental duplication. The approach should become particularly useful as high-quality alternate reference sequences become available and genome sequencing of individuals' DNA becomes more routine.

Copyright © 2012 The American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.

Rare germline large rearrangements i... [Breast Cancer Res Treat. 2012] - PubMed - NCBI

how rare are rearrangements in cancer? 

http://www.ncbi.nlm.nih.gov/pubmed/22476849

Breast Cancer Res Treat. 2012 Apr 5. [Epub ahead of print]

Rare germline large rearrangements in the BRCA1/2 genes and eight candidate genes in 472 patients with breast cancer predisposition.

Rouleau E, Jesson B, Briaux A, Nogues C, Chabaud V, Demange L, Sokolowska J, Coulet F, Barouk-Simonet E, Bignon YJ, Bonnet F, Bourdon V, Bronner M,Caputo S, Castera L, Delnatte C, Delvincourt C, Fournier J, Hardouin A, Muller D, Peyrat JP, Toulas C, Uhrhammer N, Vidal V, Stoppa-Lyonnet D, Bieche I,Lidereau R.

Source

Laboratoire d'Oncogénétique, Institut Curie-Hôpital René Huguenin, 35 rue Dailly, 92210, Saint-Cloud, France, etienne.rouleau@curie.net.

Abstract

Hereditary breast cancers account for up to 5-10 % of breast cancers and a majority are related to the BRCA1 and BRCA2 genes. However, many families with breast cancer predisposition do not carry any known mutations for BRCA1 and BRCA2 genes. We explored the incidence of rare large rearrangements in the coding, noncoding and flanking regions of BRCA1/2 and in eight other candidate genes-CHEK2, BARD1, ATM, RAD50, RAD51, BRIP1, RAP80 and PALB2. A dedicated zoom-in CGH-array was applied to screen for rearrangements in 472 unrelated French individuals from breast-ovarian cancer families that were being followed in eight French oncogenetic laboratories. No new rearrangement was found neither in the genomic regions of BRCA1/2 nor in candidate genes, except for the CHEK2 and BARD1 genes. Three heterozygous deletions were detected in the 5' and 3' flanking regions of BRCA1. One large deletion introducing a frameshift was identified in the CHEK2 gene in two families and one heterozygous deletion was detected within an intron of BARD1. The study demonstrates the usefulness of CGH-array in routine genetic analysis and, aside from the CHEK2 rearrangements, indicates there is a very low incidence of large rearrangements in BRCA1/2 and in the other eight candidate genes in families already explored for BRCA1/2 mutations. Finally, next-generation sequencing should bring new information about point mutations in intronic and flanking regions and also medium size rearrangements.

PMID:

 

22476849

 

[PubMed - as supplied by publisher]