April 28, 2011 § Leave a comment
Lea Goentoro, who is leaving the Kirschner lab shortly to set up her own lab at Caltech, is looking for post-docs to join her new group, starting in June. Lea is very curious about how a small number of signaling pathways (at most recent count, there are only 20 pathways that function in adult cells, and only 5 in development) have so many varied functions. She has provided some thoughtful musings on this topic on her new website, so that you can become curious too… here are some specific questions:
Do cells sense absolute or relative level of signal?
One pathway, many functions.
How to be a part of the whole?
Check out her position listing page for details on what kinds of applicants she’s looking for. Lea is going to be a wonderful lab head. You heard it here first.
For a snippet about Lea’s postdoctoral work, check out this post.
December 2, 2010 § Leave a comment
Phillip Niethammer from the Mitchison lab will be setting up his own lab at the Sloan Kettering Institute this January. I’ve written (briefly) about Phillip’s super-cool work in zebrafish here. The overall goal of his lab is to perform a systems level analysis of the wound response using in-vital imaging and genomic techniques in zebrafish. Here’s what he says about what he’s looking for:
My lab is interested in the question of how wounds are detected in animal tissues. I am looking for postdocs who are curious to explore the spatiotemporal mechanisms of homeostatic/inflammatory tissue signaling in zebrafish. Candidates should have an excellent track record in common molecular and microscopic techniques. They should be self-motivated, interactive and enjoy interdisciplinary thinking. Researchers with biological, biophysical, chemical, or medical backgrounds are encouraged to apply.
The lab is part of the Cell Biology Program of the Sloan Kettering Institute (New York City, USA). Rockefeller University and Cornell Medical School, across the street, provide rich opportunities for additional scientific interaction. Application documents should include a CV, publication list, short description of research experience/interests, and reference letters from previous advisors.
November 5, 2010 § Leave a comment
Eric Batchelor (Lahav lab) is in the process of setting up his new lab at the NIH and is beginning to look for post-docs. Eric has been a wonderful part of our community and we’re all sure he’s going to be a great lab head. Graduate students, take note.
Here’s his ad:
The Batchelor lab is interested in understanding how biological circuits enable cells to process information and make decisions. We focus on stress responses in mammalian cells, with particular interests in the p53 tumor suppressor network and the unfolded protein response. To understand the regulation and the function of these networks, we combine experimental and computational approaches including long-term time-lapse microscopy, chemical and genetic perturbations, and predictive modeling. We aim to not only develop a more quantitative understanding of the proper functioning of stress response networks, but also identify novel strategies to combat diseases in which stress responses are dysregulated, including cancer, diabetes, and neurological disorders.
Postdoctoral positions are available starting in May 2011. We are interested in candidates with strong backgrounds in molecular biology, cell biology, and/or quantitative sciences, who enjoy working in a collaborative environment and who are enthusiastic about using systems-level analyses to tackle questions in biological signal transduction.
To apply, email a cover letter describing your research interests, a CV, and a list of three references to email@example.com.
Eric Batchelor, Alexander Loewer and Galit Lahav. The ups and downs of p53: understanding protein dynamics in single cells. Nature Reviews Cancer 2009; 9: 371-377
Eric Batchelor, Caroline S. Mock, Irun Bhan, Alexander Loewer and Galit Lahav. Recurrent initiation: a mechanism for triggering p53 pulses in response to DNA damage. Molecular Cell, 2008; 30(3): 277-289.
Eric Batchelor and Mark Goulian. Robustness and the cycle of phosphorylation and dephosphorylation in a two-component regulatory system. Proc Natl Acad Sci USA, 2003 100, 691-696.
November 2, 2010 § 2 Comments
What is electricity? It’s moving electrons. Every living thing moves electrons around, not just in nerves (for those of us that have them) but also in metabolism (oxidize one thing, reduce another). Is it possible to use this metabolic electricity to communicate with man-made devices? If you could, you might be able to make very sensitive biosensors, or even use bacteria to charge your batteries. The first question you would need to address is whether you could get the electrons generated by metabolism out to the surface of the cell where they could be captured by a metal electrode.
October 4, 2010 § Leave a comment
Eric Deeds, who left the Fontana lab a few weeks ago to set up his own group at the Center for Bioinformatics at Kansas University, is now recruiting post-docs.
From the lab home page:
Understanding the Assembly of Macromolecular Structures
Most biological processes rely, in some form or another, on the action of large protein or protein-nucleic acid complexes. Protein synthesis, for example, is catalyzed by the ribosome, a massive molecular machine consisting of 3-4 large RNA molecules and 50-80 proteins, depending on the organism in question. Transcription, splicing, protein degradation and signaling all involve the action of similarly large complexes.
Cells do not synthesize these machines as fully formed entities, but rather as a set of components (e.g. individual proteins and nucleic acids) that must assemble into a higher-order structure in order to perform their functions. At its core, this assembly process is mediated by a set of intermolecular (binding) interactions. In our lab we use mathematical and computational modeling to examine how a set of interacting components assembles into a fully-formed macromolecular structure. We are actively considering the following areas:
- Optimizing the assembly of ring-like structures
- Understanding assembly in the context of large Protein-Protein Interaction networks
- Developing methods to allow for the design of structures that will self-assemble efficiently
Our lab also has interests in modeling the dynamics of signaling networks and in analyzing and developing models of allometric scaling. Please see our research page for more information!
August 16, 2010 § Leave a comment
Drug discovery tends to happen via one of two main ways. Either you look for a phenotypic effect — as in, chewing that willow bark eased my headache, or this fungal extract stopped my rat liver membrane prep from making cholesterol — or you look for a specific effect on a purified target. Both have disadvantages [and advantages, of course]: an effect found in a phenotypic screen may be very hard to track down to a particular small molecule, and a specific mechanism, while a purified-target assay may give you many hits that don’t turn out to be useful in the complex environment of a whole cell, let alone the human body. Now Riki Eggert’s lab has shown that there is a middle path: targeting a whole pathway (Castoreno et al. 2010 Small molecules discovered in a pathway screen target the Rho pathway in cytokinesis. Nat Chem Biol. 6 457-63 PMID: 20436488).
Castoreno et al. were interested in finding inhibitors of the Rho pathway, a complex and many-branched pathway that is at the heart of several key cellular functions such as migration, adhesion, and cytokinesis, the process by which two daughter cells separate from each other once their DNA has doubled and divided. Rho itself is a GTPase that switches between two states, GTP-bound (active) and GDP-bound (inactive). Quite a few regulatory proteins are involved in this cycle, including the Guanine nucleotide Exchange Factors (GEFs), which encourage the exchange of bound GDP for GTP, and the GTPase Activating Proteins (GAPs), which encourage cleavage of the GTP to form GDP, inactivating Rho. Active Rho has several targets, and at least three of the pathways activated by Rho converge on cytokinesis.
June 29, 2010 § 1 Comment
Now get the T-shirt. A lot of people reading this blog are members of what I’m calling the Systems Biology Diaspora, people who were in the Department as graduate students or post-docs and are now elsewhere, but remain — whether they like it or not — spiritually part of the Department. Maybe you’re in a lab run by a Diasporite. Whoever you are, we have some extra T-shirts from the Department retreat this year, and if you’d like to write in and ask for one, you can have one. Please e-mail Angela Reese and tell her what size you want. We have medium, large and XL available; offer valid until we run out. Please put “T-shirt” in the subject line of your e-mail.
The design shows the main model organisms used in the Department, in a complex network of interconnected feedback loops. The image was created by our good friend Brian Knep. (Yes, OK, it’s cheating to have a professional artist design our T-shirt. We agree. It’s still a nice T-shirt.)
The person imitating a headless horseman behind the T-shirt on the left is Kathy Buhl from Lab Ops, in case you’re curious.
Wear it with pride!
June 14, 2010 § 1 Comment
This month, we say a tearful goodbye to Julio Saez-Rodriguez. Julio is setting up his own group at the European Bioinformatics Institute (EBI) in Hinxton, near Cambridge UK, starting on July 1. EBI is a great fit for him, with its focus on developing computational tools to serve the whole biological community. There’s an added bonus in that he will be about 3,000 miles closer to his home town in Spain.
Julio came to the Department when the Sorger lab joined us from MIT. He’s been a major driver of the Sorger lab’s efforts to develop logical models that represent real cellular pathways. Much of the time, our view of a biological pathway is a kind of average, created by combining the lists of interactions identified in dozens or hundreds of cell lines. But the pathway doesn’t have to be the same in every cell type — the differences in behavior between cells have to come from somewhere, and by now we know that there are not enough genes in the human genome to allow each cell type to have whole pathways that are different from other cell types. When Julio looked at liver cells, for example (with Leo Alexopoulos), he started with a consensus model assembled from the literature of the pathways controlling the response to seven different cytokines. Using an extensive dataset of signal/response measurements taken exclusively from HepG2 cells, he asked how well the literature model could predict actual cell behavior. What he found was that in order to make the consensus pathway work, he had to drop several “proven” interactions in the network — and add several that had indeed been observed in one cell type or another, but were not sufficiently consistently observed to get into the consensus model.
One day, the signaling community will realize that Julio has done them a huge favor. Instead of fighting over who’s right and who’s wrong, everyone can be right — as long as you’re studying different cell types, or (if you get desperate) different variants of the same cell types. Studying one cell type instead of another is like entering an alternate universe: anything can happen somewhere.
Julio plans to continue to work on developing models to help us understand the logic, and the cell specificity, of signaling pathways. He’s hiring post-docs, and he’s also interested in collaborators and short-term visitors; you still have a week or so to chat to him about the possibilities. (The UK is warmer than Boston in the winter, although it has to be said that it is also grey and drizzly.)
Good luck, Julio, and keep in touch!