NTU Singapore International PhD Program in Computational Biology/ Bioinformatics

NTU Singapore International PhD Program in Computational Biology/ Bioinformatics

The scientific landscape of bioinformatics/computational biology continues to change as the field is still evolving. It is anticipated that new scientific insights in computational biology and bioinformatics will impact the continued growth in biomedical science and biotechnology and will have considerable socio-economic impact.

Nevertheless, the number of personnel with major specialization in bioinformatics/computational biology hired by academia and industry remains small; yet, the professional requirements remain high and include a thorough education in

(i) mathematics and exact natural sciences (physics/chemistry),

(ii) computer science including programming and

(iii) life sciences (especially molecular level life sciences). Since bioinformatics applications in the real world occur at the cutting edge of the field, professionals in this field need to have strong own research experience.

This is exactly the goal of the SCE-BII PhD Program in Computational Biology and Bioinformatics.

PhD. student opportunities at the Bioinformatics Institute of the Agency for Science, Technology and Research (A*STAR) have so far been provided only by the A*STAR Graduate Academy. There are the NSS and AGS programs for applicants from Singapore and the SINGA program for some international applicants.

In March 2010, BII has entered a Memorandum of Understanding (MOU) with the School of Computer Engineering of the Nanyang Technological University (NTU-SCE) to support a newly established PhD. program in Computational Biology and Bioinformatics administered by NTU-SCE, with this step crowning the long-standing partnership of both sides. This support involves block-funding from BII as well as support with teaching and research resources.

Under this program, there will be multiple up-to-4-year scholarships to train graduates (with a Master of Science in natural sciences or engineering) towards a PhD. in Computational Biology and Bioinformatics. Besides a limited set of coursework aimed at complementing the existing knowledge of the applicant in an interdisciplinary manner, involvement in actual research as a member of a research team at BII or SCE will be the main activity during the training.

Applicants with excellent results during their university studies and a strong interest in computational biology/bioinformatics research are encouraged to apply. There are no eligibility limitations other than good performance, and applications from Singapore, countries in Southeast Asia or anywhere in the world are considered on a purely meritocratic basis.

How to Apply:

Kindly download the application form and email a completed form toscebii@bii.a-star.edu.sg.

Applicants to this PhD. program are expected to have completed a full Master of Science Program in natural sciences or engineering in a related field such as biology, chemistry, physics, computer science or medicine when the PhD. is started.

Dominant prion mutants induce curing through pathways that promote chaperone-mediated disaggregation

Protein misfolding underlies many neurodegenerative diseases, including the transmissible spongiform encephalopathies (prion diseases). Although cells typically recognize and process misfolded proteins, prion proteins evade protective measures by forming stable, self-replicating aggregates. However, coexpression of dominant-negative prion mutants can overcome aggregate accumulation and disease progression through currently unknown pathways. Here we determine the mechanisms by which two mutants of the Saccharomyces cerevisiae Sup35 protein cure the [PSI⁺] prion. We show that both mutants incorporate into wild-type aggregates and alter their physical properties in different ways, diminishing either their assembly rate or their thermodynamic stability. Whereas wild-type aggregates are recalcitrant to cellular intervention, mixed aggregates are disassembled by the molecular chaperone Hsp104. Thus, rather than simply blocking misfolding, dominant-negative prion mutants target multiple events in aggregate biogenesis to enhance their susceptibility to endogenous quality-control pathways.

Figures at a glance

left

1. Figure 1: PNM mutants are distinguished by their effective inhibitory ratios.

   

   (a) Wild-type (HSP104/HSP104) or heterozygous-disruption (HSP104/Δ) diploid strains expressing wild-type (WT) and PNM mutants (Q24R, G58D) from P₃₅ at the indicated ratios were spotted on rich (1/4 YPD) or adenine-deficient (−ADE) media to analyze the [PSI⁺] phenotype. Wild-type [PSI⁺] and [psi⁻] diploids (74-D694) were included as controls. (b) To determine the frequency of prion loss, wild-type meiotic progeny (n ≥ 19 for each strain) were isolated from the diploids described in a, and the percentage of [psi⁻] colonies was determined.

2. Figure 2: PNM mutants incorporate into wild-type aggregates and alter multiple events in prion propagation.

   

   (a) HA-tagged Sup35 (WT or mutants) expressed from P₃₅ in haploid [PSI⁺] (+) or [psi⁻] (−) yeast strains, which also expressed untagged Sup35, was immunoprecipitated with anti-HA serum (Ab) and analyzed by SDS-PAGE and anti-Sup35 immunoblotting. (b) [psi⁻] haploids expressing Sup35 (WT or mutants) from P₃₅ and a fluorescent reporter of translation termination efficiency (GST-UGA-DsRed-NLS) were mated to wild-type [PSI⁺] or [psi⁻] (74-D694) cells, and the percentage of fluorescent zygotes was scored. Error bars represent s.d. from three independent experiments, each analyzing at least 15 zygotes per cross (*P = 0.039 in comparison with WT). (c) The fluorescence intensities of zygotes isolated from the indicated crosses as described in b were determined. Horizontal lines on boxes indicate 25th, 50th and 75th percentiles; error bars indicate 10th and 90th percentiles; dots represent outliers (n ≥ 30; *P = 0.0009). (d) Lysates from wild-type haploid strains expressing an additional copy of Sup35 (WT or mutants) from P_tetO2 were incubated in SDS at the indicated temperatures before SDS-PAGE and quantitative immunoblotting for Sup35 (percentage of Sup35 at the indicated temperatures relative to 100 °C). Error bars represent s.d. (n ≥ 6, *P = 0.0003, **P = 0.0001, ***P = 0.008 in comparison with WT at the same temperature).

3. Figure 3: PNM mutants alter the accumulation of propagons but not their transmission.

   

   (a) Lysates from haploid wild-type yeast strains expressing Sup35 (WT or mutants) from P_tetO2 were analyzed by SDD-AGE and immunoblotting for Sup35. Wild-type [PSI⁺]^Strong, [PSI⁺]^Weak and [psi⁻] yeast strains are shown as controls. (b) The number of propagons present in individual cells was determined for the indicated strains, as described in a. Horizontal lines on boxes indicate 25th, 50th and 75th percentiles; error bars indicate 10th and 90th percentiles; dots represent outliers (n ≥ 39; *P ≤ 0.0001 in comparison with WT). (c) The proportion of Sup35 transmitted to daughter cells (circles) or to mother cells (squares) was determined by fluorescence loss in photobleaching (FLIP) of a [PSI⁺] strain expressing Sup35-GFP alone ([PSI⁺]) or with a second copy of Sup35 (WT-GFP + WT) or G58D (WT-GFP + G58D) from P_tetO2. Error bars represent s.e.m. from three independent experiments, each analyzing at least 10 cells.

4. Figure 4: PNM expression promotes Hsp104-mediated disassembly of aggregates.

   

Several positions@ CDAC, India

Centre for Development of Advanced Computing (C-DAC) invites online applications from skilled and experienced professionals from the interdisciplinary domain of Information & Communication Technologies for the following areas of operations: http://www.cdac.in/html/jobs/pune_may2011.asp

Courtesy:  Dr. Jayaraman Valadi

POSITIONS:
All the positions are on contract for a fixed duration and against approved projects. No of posts advertised may vary as per the project requirements with consolidated pay as per C-DAC norms.

AGE:
Maximum age limit will vary according to the experience asked for the post. Applicants belonging to the reserved category / Govt. employees would be eligible for relaxations according to the Government of India’s norms.

Last date of advertisement is May 30, 2011. (6:00 PM)

HOW TO APPLY:
Please apply online by clicking the appropriate link above.

Applicants working in Central/State Govt/PSU or any Govt Undertaking are required to forward an online advance copy of the application and submit the applications through the proper channel by clearly mentioning the position code on the application.

HRD – Recruitment
Center for Development of Advance Computing
NSG IT Park, S. No. 127/2B/2A,
Sarja Hotel Lane, Aundh, Pune – 411 007,
Tel: +91-20-25503100/01/02
Fax: + 91-20-25503131

Note: I. Applicants need to apply for only one position. Applicant who applies for multiple positions will not be considered for any position.
II.Those who are appearing for the final exam of Degree need not apply. (except Junior Research Fellow position)

RFI: Whole Genome Sequencing, Data Analysis, Storage and Annotation

The National Institute of Neurological Disorders and Stroke is considering how next-generation genome sequencing (NGS) will be applied in studies of neurological disorders, and is asking researchers in this area for information about how they plan to use the latest sequencing tools and genomic data in their work.


To find out how researchers aim to use next-gen whole genome sequencing (WGS), and what the needs are for sequencing, data storage, analysis, and annotation services, NINDS has released a new request for information seeking feedback from the extramural research community.


NINDS will use this feedback to inform and complement its efforts to assess the current and future whole genome sequencing needs of researchers studying a wide range of neurologic disease, and conducting basic research into the nervous system, the genetics of the brain, cognition, brain plasticity, neural signaling, learning, memory, motor control, and other areas.

Bioinformatics helps identify TIM-1 as the receptor for Zaire Ebolavirus and Lake Victoria Marburgvirus

The glycoproteins (GP) of enveloped viruses facilitate entry into the host cell by interacting with specific cellular receptors. Despite extensive study, a cellular receptor for the deadly filoviruses Ebolavirus and Marburgvirus has yet to be identified and characterized. Here, we show that T-cell Ig and mucin domain 1 (TIM-1) binds to the receptor binding domain of the Zaire Ebola virus (EBOV) glycoprotein, and ectopic TIM-1 expression in poorly permissive cells enhances EBOV infection by 10- to 30-fold. Conversely, reduction of cell-surface expression of TIM-1 by RNAi decreased infection of highly permissive Vero cells. TIM-1 expression within the human body is broader than previously appreciated, with expression on mucosal epithelia from the trachea, cornea, and conjunctiva—tissues believed to be important during in vivo transmission of filoviruses. Recognition that TIM-1 serves as a receptor for filoviruses on these mucosal epithelial surfaces provides a mechanistic understanding of routes of entry into the human body via inhalation of aerosol particles or hand-to-eye contact. ARD5, a monoclonal antibody against the IgV domain of TIM-1, blocked EBOV binding and infection, suggesting that antibodies or small molecules directed against this cellular receptor may provide effective filovirus antivirals.

supporting matirial

Using a bioinformatics screen, the team found clues that a protein encoded by the T-cell immunoglobulin and mucin domain 1 gene TIM-1 serves as a receptor for the Ebola virus strain Zaire ebolavirus in some cell types. Through a series of follow-up functional studies, they verified this interaction and showed that TIM-1 can also act as a cellular port of entry for another hemorrhagic-fever causing virus: Lake Victoria marburgvirus.


Because TIM-1-expressing cells seem to turn up in some tissues most vulnerable to Ebola and Marburg infection, researchers say, the findings hint that targeting TIM-1 might eventually help prevent some hemorrhagic infections, since their experiments suggest blocking the receptor prevents Ebola movement into cells expressing the receptor.


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A thorough discussion about personal genomics - Personalized Perspectives

A thorough discussion about personal genomics — what it means for the average consumer, the health care system, and the research community often raises more questions than it answers. While the public discourse on genetic privacy can be traced back to the days of the Human Genome Project, only recently has a new era been ushered in thanks to the steady decrease in the cost of DNA sequencing with promises of a tailor-made approach to medical treatment and new discoveries from rich genetic data sets. Depending on whom you ask, personal genetic information should either be protected at all costs as personal property or is merely information fit to published online for the whole world to see and contains nothing more revealing about health than, say, the knowledge that someone smokes.

That there is such concern over whether genetic information is more vulnerable to attack or misuse than traditional personal health care records may be an unintended consequence of the hype that touted personal genomics as a means to discover all there is to know about a person. "We've done it to ourselves. The way we were selling this idea of genomic data providing much better insight into who you are, and your future, than all other types of data it was very effective and we really meant it," says Misha Angrist, an assistant professor at Duke University's Institute for Genome Sciences and Policy. "However, until we find all that dark inherited matter that we haven't identified to date, most of our genomic signals are not nearly as disclosing as knowing your health risks because you're a smoker. But you can imagine that if one wanted to be a bit worried about the health care system, having a whole community saying that we're going to [be] developing the preeminent disclosing data source, people who were likely to get scared were going to get scared."

During the first few months of 2011 alone, advocacy groups like the Forum for Genetic Equity, concerned citizens, and a handful of state representatives began efforts to protect personal genetic information. In January, a group of Massachusetts state senators introduced the Massachusetts Genetic Bill of Rights in an attempt to make up for perceived shortcomings of the federal US Genetic Information Nondiscrimination Act of 2008. "This is a new era in medicine and we need to make sure that [there are] some sort of safeguards. We thought it would be important to deal with this quickly, rather than at some future time after perhaps people had already lost some of their rights," says Massachusetts Senator Harriette Chandler, who is a lead sponsor of the bill. "There obviously are issues; the insurance industry is not going to like this because they feel that they want to know any genetic information that the individual has, but what we're trying to say is that basically genetic information is your property, like any other property you have, and you have a right to privacy with respect to genetic material."

In March, representatives in Vermont and California introduced similar bills in an attempt to declare genetic information the exclusive property of the individual, among other protections. These bills face many hearings and debate sessions before having a chance of being enacted into law, but the movement is expected to spread across the country.

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