25 Essential Free Palm Pre Apps for Fitness and Exercise

25 Essential Free Palm Pre Apps for Fitness and Exercise

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Biotech Roundup: Wednesday, November 4

Biotech Roundup: Wednesday, November 4

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Top 50 Biotech Blogs

Top 50 Biotech Blogs

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Inefficient Selection: New Evolutionary Mechanism Accounts For Some Of Human Biological Complexity

We have found a specific evolutionary mechanism to account for a portion of the intricate biological complexity of our species," said Ariel Fernandez, professor of bioengineering at Rice University. "It is a coping mechanism, a process that enables us to deal with the fitness consequences of inefficient selection. It enables some of our proteins to become more specialized over time, and in turn makes us more complex."

Fernandez is the lead author of a paper slated to appear in the December issue of the journalGenome Research. The research is available online now.

Fernandez said the study drew from previous findings by his own research group and from seminal work of Michael Lynch, Distinguished Professor of Biology at Indiana University and a recently elected a fellow of the National Academy of Science. Lynch's work has shown that natural selection is less efficient in humans as compared with simpler creatures like bacteria. This "selection inefficiency" arises from the smaller population size of humans as compared with unicellular organisms.

"In all organisms, genes get duplicated every so often, for reasons we don't fully understand," Fernandez said. "When working efficiently, natural selection eliminates many of these duplicates, which are called 'paralogs.' In our earlier work, we saw that an unusual number of gene duplicates had survived in the human genome, which makes sense given selection inefficiency in humans."

In prior research on protein structure, Fernandez's team found that some proteins are packaged more poorly than others. Moreover, they found that the least-efficiently packed proteins are structurally stable only when they bind with partner proteins to form complexes.

"These poorly packed proteins are potential troublemakers when gene duplication occurs," Fernandez said. "The paralog encodes more copies of the protein than the body needs. This is called a 'dosage imbalance,' and it can make us sick. For instance, dosage imbalance has been implicated in Alzheimer's and other diseases."

Given selection inefficiency, Fernandez knew that paralogs encoding poorly packed proteins could remain in the human genome for quite a while. So he and graduate student Jianpeng Chen decided to examine whether gene duplicates had remained in the genome long enough for random genetic mutations to affect the paralogs dissimilarly. Fernandez and Chen, now a senior researcher in Beijing, China, cross-analyzed databases on genomics, protein structure, microRNA regulation and protein expression in such troublesome paralogs.

"The longer these duplicate genes stick around due to inefficient selection, the more likely they are to suffer a random mutation," Fernandez said. "Portions of every gene act to regulate protein expression -- by binding with microRNA, for example. We found numerous instances where random mutations had caused paralogs to be expressed dissimilarly, in ways that removed detrimental dosage imbalances."

Lynch said one aspect of Fernandez's research that is potentially groundbreaking is the observed tendency of proteins to evolve a more open structure in complex organisms.

"This observation fits with the general theory that large organisms with relatively small population sizes -- compared to microbes -- are subject to the vagaries of random genetic drift and hence the accumulation of very mildly deleterious mutations," Lynch said.

In principle, he said, the accumulation of such mutations may encourage a slight breakdown in protein stability. This, in turn, opens the door to interactions with other proteins that can return a measure of that lost stability.

"These are the potential roots for the emergence of novel protein-protein interactions, which are the hallmark of evolution in complex, multicellular species," Lynch said. "In other words, the origins of some key aspects of the evolution of complexity may have their origins in completely nonadaptive processes."

Fernandez said the research reveals how increasingly specialized proteins can evolve. He drew an analogy to a business that hires two delivery drivers that initially cover the same parts of town but eventually specialize to deliver only to specific neighborhoods.

"Eventually, even if times become tough, you cannot lay off either of them because they each became so specialized that your company needs them both," he said.

The more simple a creature is, the fewer specialized proteins it possesses. Humans and other higher-order mammals need many specialized proteins to build the specialized tissues in their skin, skeleton and organs. Even more specialized proteins are needed to maintain and regulate them. This complexity requires that the duplicates of the original jack-of-all-trades gene be retained, but this does not happen unless selection is inefficient. This is frequently a point of contention between proponents of evolution and intelligent design.

Fernandez and Chen looked at duplicate genes across the human genome and found that the more poorly packed a protein was, the more likely it was to be distinguished through paralog specialization.

"This supports the case for evolution because it shows that you can drive complexity with random mutations in duplicate genes," Fernandez said. "But this also implies that random drift must prevail over Darwinian selection. In other words, if Darwinian selection were ruthlessly efficient in humans -- as it is in bacteria and unicellular eukaryotes -- then our level of complexity would not be possible."

The research is supported by the National Institutes of Health.

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Protein p53 plays three cancer-fighting roles

A new study shows this cancer-controlling protein, p53, does not one, not two, but three different jobs, all in one convenient package.

Previous studies have demonstrated that p53 stops cancer from developing by sensing stress, such as DNA damage, and turning on genes that keep cells from dividing until the damage is repaired. The protein, which is a normal component of cells, also teams up with other molecules to trigger apoptosis, a type of cellular suicide, in over-stressed cells.

And now, researchers from University of Tokyo and their colleagues report in the July 23 Nature that p53 helps slice long pieces of RNA into small regulatory molecules called microRNAs. These microRNAs help control production of proteins, including some involved in cell proliferation, which can lead to cancer if unchecked.

This newly discovered function for p53 is "really surprising," says Franck Toledo, a geneticist at the Curie Institute's research center in Paris. Toledo and others have studied p53's other two roles, but no one previously suspected the protein might also participate in the slicing and dicing of RNAs.
All three of the cancer-related functions require a part of the protein that latches on to specific DNA sequences. Most cancers have some disruption in p53's action, either a mutation or inactivation of the protein, Toledo says. In many tumors, the mutation lies in the portion of p53 called the DNA-binding domain.

Scientists thought that p53 could direct the production of long RNAs, called primary transcripts, which eventually are broken up into microRNAs. Previous work has shown that the protein turns on production of a long RNA molecule that gets chopped into a microRNA called miR-34.
Mutations in the protein would disrupt production of the primary transcripts, ultimately leading to lower levels of microRNAs. But the Japanese team found that primary transcripts of several microRNAs associated with cancer are made as usual in DNA-damaged cells, indicating that p53 doesn't play a role in their production. But it was still possible that p53 mutations might disrupt the machinery that chops RNA into microRNA, says Kohei Miyazono, a molecular biologist at the University of Tokyo.

In the new study, Miyazono and colleagues also show that p53's DNA-binding domain interacts with Drosha and p68, proteins in an assemblage responsible for snipping primary transcripts into hairpin-shaped molecules. Another group of proteins, which includes the protein Dicer, chops the hairpins into the final, mature microRNAs. Levels of both the hairpin-shaped intermediates and mature microRNAs were lower in cells in which p53 was mutated, the team found.

Some of the affected microRNAs that the researchers examined control production of proteins involved in cell proliferation. Having too little of these microRNAs could allow too much of these growth-promoting proteins to be made, leading to uncontrolled growth and cancer.

The normal form of p53 serves as a molecular matchmaker, bringing Drosha and p68 together slightly more efficiently than the two proteins find each other on their own, the researchers showed. But altered forms of p53 spirit away p68, interrupting its interaction with Drosha.

People who have low levels of p53 develop cancer earlier and have poorer prognoses after treatment, Toledo says. It is possible that other variations in the protein may affect the ability to process microRNAs, which could make some people more vulnerable to cancer, he says. The new "findings suggest that, in human cancers, mutations that affect the DNA-binding domain of p53 essentially perform a hat trick by hitting three tumor-suppressive functions at once," Toledo and colleague Boris Bardot, also at the Curie Institute, write in a commentary published in the same issue of Nature.
Miyazono says p53 is clearly important in cancer cells, but might not be as crucial for microRNA processing in normal cells. The protein's function might be performed by other proteins in normal cells, he suggests. His group is working on different components of the microRNA-processing machinery, so other researchers will have to figure out p53's normal role in making microRNAs.
Still, he thinks the findings could have clinical applications if researchers can find ways to restore mutated or inactivated p53 to normal function.

Original report was modified by Jakub Málek.
Source: www.sciencenews.org

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Slicing chromosomes leads to new insights into cell division

By using ultrafast laser pulses to slice off pieces of chromosomes and observe how the chromosomes behave, biomedical engineers at the University of Michigan have gained pivotal insights into mitosis, the process of cell division.

Their findings could help scientists better understand genetic diseases, agingand cancer.

Hunt’s group hypothesized that polar ejection forces should be proportional to the chromosome’s size, and therefore could be predictably changed by altering the size of the chromosomes. Using newts as a model organism, they cut off pieces of the chromosomes’ arms.

More on www.ns.umich.edu

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some usefull links for forensic science elective for 7th sem under vtu syllabus

1) http://www.aafs.org

2)http://www.utica.edu/academic/institutes/ecii/ijde

3)https://www.auerbach-publications.com/home.asp

4)http://www.allstateinvestigation.com/top-ten-signs-of-a-cheater.html

5)http://www.navigantconsulting.com/services/discovery_services

6)http://www.computer-forensic.com/index.html

7)http://www.iacis.com

8)http://www.respond.com/contryguides/1800000002/NJ/023

9)http://www.canberra.edu.au/home

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winter school on bioinformatics

KERALA AGRICULTURAL UNIVERSITY
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Winter School
On
Bioinformatics and its Applications in Agriculture
1st December to 21st December, 2009 (21 days)

Sponsored by
Indian Council of Agricultural Research
New Delhi

Bioinformatics Centre (DIC)
IT-BT Complex
College of Horticulture
Kerala Agricultural University
Thrissur - 680 656, Kerala
About the subject and programme
Bioinformatics is a new emerging field that helps in collecting, linking, and manipulating different types of biological information to discover new biological insights. In short, bioinformatics is an information management system for molecular biology, biotechnology, medicine and agriculture. The most pressing tasks in bioinformatics involves the finding of genes in the DNA sequences of various organisms, developing methods to predict the structure and/or function of newly discovered proteins and structural RNA sequences, clustering protein sequences into families of related sequences ,development of protein models, aligning similar proteins and generating phylogenetic trees to examine evolutionary relationships.
The sequencing of the genomes of microbes, plants and animals should have enormous benefits for the agricultural community. Computational analysis of these sequence data generated by genome sequencing, proteomics and array-based technologies is critically important. Bioinformatics tools can be used to search for the genes within these genomes and to elucidate their functions. This specific genetic knowledge could then be used to produce stronger, more drought resistant, disease resistant, insect resistant and more productive crops.
Keeping in view the changed scientific scenario in the post-genomic era and to expose the agricultural scientists to the latest computational biology tools for biological research, a Winter School on “Bioinformatics and its Applications in Agriculture” is being organized at the Bioinformatics Centre (DIC), Kerala Agricultural University from December 1st to December 21st 2009. The training includes theory and hands-on sessions on different aspects.
About us
The Bioinformatics Centre (DIC) at Kerala Agricultural University runs under the Biotechnology Information System Network (BTISnet) programme of DBT, Ministry of Science & Technology, Government of India. The Centre was established as the 23rd Distributed Information Sub Centre (DISC) in 1995 under BTISnet programme and upgraded to DIC during 2004 to promote Bioinformatics research and education. We specialize in plant biotechnology related research work. The Centre enhances access to global information in life sciences especially plant sciences and plant biotechnology involving scientists and students of the University, other S&T institutions and acts as a support centre to the Centre for Plant Biotechnology & Molecular Biology. The Centre is involved in a wide range of research work on plants using systems biology approaches, plant-pathogen interaction studies and study of active compounds in medicinal plants. In addition to this, the Centre offers a credit course in Bioinformatics to post graduate Plant Biotechnology students, conducts various training programmes in Bioinformatics and maintains several databases relevant to agriculture.
Objectives
This program comprises of basic and advanced study domains of Bioinformatics, which are expected to equip the Scientists with a complete practical and applied knowledge
Course content
Bioinformatics and Agriculture.
Internet and search engines
Databases and internet resources for Bioinformatics analysis
Similarity search and sequence alignment
Primer Designing for gene amplification
Genomics & Proteomics
Biodiversity Informatics
Molecular Markers in crop improvement
Software for Molecular Marker Analysis
Database creation
Data mining in Bioinformatics
Bioinformatics implications in Agriculture
E-resources and E-portals in Agriculture
IPR issues in Bioinformatics
Eligibility
This Winter School is meant for young active researchers I teachers in the rank of Assistant Professor I Junior Scientist / Scientist or above having a minimum of 2 years research / teaching experience in SAUs / ICAR institutes and being actively engaged in work related to Biotechnology and Molecular Biology or any other related discipline. Applicant should not be more than 45 years of age. The total number of participants shall be limited to 25.
Venue
Bioinformatics Centre (DIC), IT – BT Complex, College of Horticulture, Kerala Agricultural University, Vellanikkara, Thrissur, Kerala.
How to reach
Thrissur is well-connected by rail and road. Cochin International Air Port is 60 km away from Thrissur. The campus is 10 km from Thrissur town towards Palghat, on NH 47
Duration
December 1 - December 21, 2009 (21 days)
Travel and other arrangements
Boarding and lodging arrangements for the participants will be provided by KAU as per the provisions of ICAR. TA will be paid on actual basis, as per the entitlement, restricted to AC – II tier rail fare, limited to the availability of funds.
Applications to be sent to:
Dr. R. Keshavachandran
Professor & Coordinator
Course Director, Winter School
Bioinformatics Centre (DIC), IT-BT Complex
Kerala Agricultural University, Vellanikkara
KAU P.O, Thrissur, Kerala. PIN 680656.
E-mail: winterschooldic@gmail.com
kaubioinfo@gmail.com
kauniv.btisnet@nic.in
For more details about Bioinformatics Centre (DIC)
Visit our Website: www.kaubic.in
Phone: 0487 – 2371994, Fax: +91 487 2371994
Procedure for registration:
The participants are required to pay a sum of Rs.50/-(Rupees fifty only) as registration fee. The fee must be paid along with the application form, in the form of postal order drawn in favour of the Associate Dean, College of Horticulture payable at KAU Post Office before 31st October, 2009.
Application form can be downloaded from the here (MS Word, 62KB)
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