MolBio Research Highlights hits the news

Those who follow me on twitter know that a few weeks ago I was interviewed by a nation-wide newspaper to discuss scientist-written blogs, particularly those arising from Chile^1,2.
Briefly, I commented that there are different types of these blogs, ranging from the ones that discuss science in general and are directed to a broad, though science-interested audience, to blogs written specifically for other scientists in a particular field (like MolBio Research Highlights).

I consider this interview (which was published today and also features María José Navarrete Talloni's blog over at Nature Network) to be timely and reflects how more and more scientists are getting on board with blogging and many are joining online communities (twitter, friendfeed, facebook, etc.) to do what we like the most: discuss science, particularly in a friendly and relaxed environment .

The article is a good way to spread the news to other Chilean scientists for them to join these communities, follow or write their own blogs and start experiencing this new way of science communication and networking.


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¹The article is entitled "We can now add blogs, to microscopes and test tubes" and was published today in "El Mercurio". It was written by Paula Leighton.

² The picture is also part of the same interview. I should really do something about that mess on my bench.

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Rant by fellow blogger: manuscript reviewing

So I'm all alone in the lab right now, waiting for what has to be, the longest PCR run in history.

Anyway, I started catching up on my blog-reading in the meantime ('cause I'm not in the mood to pick up the latest article from Steve Kay's lab just yet) and I found just what I needed: a hilarious rant by Professor in Training (you should subscribe to PiT's RSS, and while on it, subscribe to drdrA's too) :

I must admit it was difficult not to laugh while trying to find a diplomatic way of saying that the manuscript was the scientific equivalent of vomit and that it appeared to have been conceived, executed and written by a turnip.

I'm still laughing...

[Image credit: writeanovelfast]

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No T-cell left behind, an explanation to why we sleep and more in my picks of the week from RB

Another week has gone by and some very interesting molbio blog posts have been aggregated into Researchblogging.org. Every week [see my opening post on the matter], I'll select some blog posts I consider particularly interesting in the field of molecular biology [see here to get a sense of the criteria that will be used], briefly describe them and list them here for you to check out.

Note that I'm only taking into consideration the molbio-related blog posts aggregated under "Biology".

Three blog posts were selected this week:

1) The diversity of antigen receptors expressed by T-cells is enormous. The amount, then, of T-cells expressing a specific receptor for a particular antigen is very low (apparently less than 1 in 10⁵ cells). The vast expansion of specific T-cells we see a few days after an infection is the result of two processes: 1) Clonal selection, which refers to the recognition of this particular antigen by a specific (and small) subset of naïve T-cells and 2) Clonal expansion, which refers to a massive expansion of these selected clones after recognition, which gives rise to a population large enough to try to fight the pathogen. A question arises, then: when we do see clonal expansion, does this result from the recognition of the antigen by all the T-cells specific for the presented antigen, or only from a small subset of these that randomly (and luckily) interacted with the presenting cell?

Ian York (a regularly highlighted blogger in my picks of the week) discusses a recent article reporting that apparently clonal selection is extremely efficient and almost all the T-cells that potentially can recognize the particular antigen, do and expand.

2) Despite the vast amount of evidence behind AIDS research, there are still some groups denying the fact that HIV is the causative agent of AIDS.
Ben Vincent presents his ideas regarding the effects this “denialism” can have on the population and discusses “trust” in science.

3) This next blog post piqued my interest as my research focuses on circadian biology. Why do we sleep? Does it play a restorative function? Neuroskeptic discusses a recent review article proposing an alternative idea: that the evolutionary function of sleep is simply to ensure that animals are only active when the benefits of movement outweigh its costs and not because it’s physiologically needed. In other words, you’ll be active only when it’s useful for you to be active. Be sure to check the comments section for provocative discussions!

That's it for this week. Stay tuned for more MolBio Research Highlights!

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Some of the articles discussed in this week's selected posts:

van Heijst, J., Gerlach, C., Swart, E., Sie, D., Nunes-Alves, C., Kerkhoven, R., Arens, R., Correia-Neves, M., Schepers, K., & Schumacher, T. (2009). Recruitment of Antigen-Specific CD8+ T Cells in Response to Infection Is Markedly Efficient Science, 325 (5945), 1265-1269 DOI: 10.1126/science.1175455

Ascher, M., Sheppard, H., Jr, W., & Vittinghoff, E. (1993). Does drug use cause AIDS? Nature, 362 (6416), 103-104 DOI: 10.1038/362103a0

Nattrass, N. (2008). AIDS and the Scientific Governance of Medicine in Post-Apartheid South Africa African Affairs, 107 (427), 157-176 DOI: 10.1093/afraf/adm087

Siegel, J. (2009). Sleep viewed as a state of adaptive inactivity Nature Reviews Neuroscience, 10 (10), 747-753 DOI: 10.1038/nrn2697

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September and Circadian Clocks

September has been a fascinating month for circadian biology. Some very interesting articles have been published, derived from studies on typical model organisms used in chronobiology. Some are very recent, as you'll notice.

Particularly related to my research, the Liu Lab published a provocative paper on the role of the exosome in the Neurospora circadian system (and may have a role in other organisms, too) , and a nice review from the Dunlap Lab focuses on post-translational modifications affecting core functions of eukaryotic clocks, "in particular the functionally related oscillators in Neurospora crassa, Drosophila melanogaster, and mammalian cells".

Generally, there are just a few articles on the subject per month among the journals I usually follow, so this is really exciting.

I'll just list some of them here for you to check out:

Steve Kay's Lab: A Genome-wide RNAi Screen for Modifiers of the Circadian Clock in Human Cells. Cell, 18 September 2009

Michael Brunner's Lab: Phosphorylation modulates rapid nucleocytoplasmic shuttling and cytoplasmic accumulation of Neurospora clock protein FRQ on a circadian time scale. Genes & Dev. 2009. 23: 2192-2200

Michael Rosbash's Lab: A role for microRNAs in the Drosophila circadian clock. Genes Dev. 2009 Sep 15;23(18):2179-91.

Yi Liu's Lab: The Exosome Regulates Circadian Gene Expression in a Posttranscriptional Negative Feedback Loop. Cell, Volume 138, Issue 6, 1236-1246

Jay Dunlap's Lab: Post-translational modifications in circadian rhythms. Trends Biochem Sci. 2009 Sep 7

Frank Weber's Lab: Sequential and Compartment-specific Phosphorylation Controls the Life Cycle of the Circadian CLOCK Protein. J Biol Chem. 2009 Aug 28;284(35):23734-42

Yoshitaka Fukada's Lab: Preferential Inhibition of BMAL2-CLOCK Activity by PER2 Reemphasizes Its Negative Role and a Positive Role of BMAL2 in the Circadian Transcription. JBC 284: 25149-25159.

Enjoy!

[Image by photomastergreg]

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Ninja viruses, a (free) radical take on aging and more in my picks of the week from RB

Another week has gone by and some very interesting molbio blog posts have been aggregated into Researchblogging.org. Every week [see my opening post on the matter], I'll select some blog posts I consider particularly interesting in the field of molecular biology [see here to get a sense of the criteria that will be used], briefly describe them and list them here for you to check out.

Note that I'm only taking into consideration the blog posts aggregated under "Biology".

This week, three blog posts made the list:

1. For them to be “successful”, viruses must be able to cope with the host’s immune system: they must evade defense responses. Viruses possess a series of “immune evasion genes” that help them do just that. Influenza, as expected, also has its own set of immune evasion genes, the most important one being the NS1 gene, which blocks the interferon pathway. We know NS1 is important for the virus, as recombinant influenza viruses lacking the NS1 protein are incapable of replicating efficiently in immunocompetent animals. We also know, however, that interferon is important in the antiviral response against influenza, so:

(…) there’s a bit of a paradox here. We know that NS1, the interferon blocker, is important to influenza virus. But we also know that interferon is very important in controlling influenza virus infections. For example, mice that can’t respond to interferons are much more susceptible to infection with avian influenza. So if NS1 works by blocking interferon, why does interferon still protect?

Ian York at Mystery Rays from Outer Space, discusses a recent article¹ shedding light on this apparent contradiction. It looks like NS1 helps to keep influenza in "a time-limited 'stealth phase' during which the replicating influenza virus remains undetected, thus preventing the immediate initiation of innate and adaptive immunity". Apparently, it may all be about timing.

2. The widely known “mitochondrial free radical theory of aging”, states that “the macromolecular damage that results from the production of toxic reactive oxygen species (ROS) during cellular respiration is the cause of aging”²

Chris Patil at Ouroboros sets the frame for an interesting discussion: is this theory still valid? Chris comments on a recent review arguing that it should be to put to rest, while also directing us to some of his previous (and fascinating) posts on the subject, to exemplify that there’s still no final say on the matter:

I doubt very much that this article will put a permanent end to the controversy. Data reported fairly recently have breathed new life into oxidative theories in general and the MFRTA in particular.

3) Finally, I'd also like to highlight a nice post from our very own Francisco Barriga, who discusses a recent article³ from Bob Weinberg's lab, where a high-throughput screen to identify chemical agents that could selectively target cancer stem cells, is presented.

Despite the excitement such a study can generate, Pancho calls for caution:

Only time will tell if the CSC hypothesis holds true for all or certain types of tumors and whether if this has any clinical relevance.

That's it for this week. Stay tuned for more MolBio Research Highlights!

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Some of the articles discussed in this week's selected posts:


¹Moltedo, B., Lopez, C., Pazos, M., Becker, M., Hermesh, T., & Moran, T. (2009). Cutting Edge: Stealth Influenza Virus Replication Precedes the Initiation of Adaptive Immunity The Journal of Immunology, 183 (6), 3569-3573 DOI: 10.4049/jimmunol.0900091

²Lapointe, J., & Hekimi, S. (2009). When a theory of aging ages badly Cellular and Molecular Life Sciences DOI: 10.1007/s00018-009-0138-8

³Gupta, P., Onder, T., Jiang, G., Tao, K., Kuperwasser, C., Weinberg, R., & Lander, E. (2009). Identification of Selective Inhibitors of Cancer Stem Cells by High-Throughput Screening Cell, 138 (4), 645-659 DOI: 10.1016/j.cell.2009.06.034

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Targeting cancer stem cells: chemical style

In a previous post I tried to summarize the major points underlying the Cancer Stem Cell Hypothesis, which states that tumors are hierarchically structured and that a particular subpopulation of cells, cancer stem cells (CSCs), are capable of initiating and sustaining the growth of the tumor [Cancer Stem Cells: the root of all evil?]. This has obvious clinical implications since eliminating these cells would lead to the definitive disappearance of the tumor.

A recent issue of Cell featured an article addressing one of the major questions in cancer biology nowadays: can we selectively target cancer stem cells within the whole tumor?

This paper tries to answer this question by developing a high-throughput screening method to identify chemical agents that could selectively target the CSC population within the tumor. This is a technically challenging matter to address since CSCs have been reported to be a very small subpopulation within the tumor and hard to maintain in culture.

To circumvent these problems, the authors sought to enrich CSCs in a cultured breast cancer cell line. They performed this by inducing a mesenchymal phenotype on the cells, a phenomenon known as epithelial to mesenchymal transition (EMT). This was based on a previous publication from the same group (Mani et al, 2008), where they showed that EMT-induced cells are enriched in all the phenotypical features of CSCs.

After setting this "CSC culture" up, they screened ~16,000 compounds for their effects on these cells and control ones (that is, EMT-induced and control cells).

The screen revealed that about 10% of the compounds had an effect on the viability of both cell populations. Interestingly, they found that 32 compounds showed selective toxicity on the CSC population and had no effect on the control cells (which could be considered as “bulk” population, see Cancer Stem Cells: the root of all evil?). From these 32, only 4 showed consistent evidence of selective toxicity on these cells and they decided (mainly because of availability issues ,as they claim) to continue their work with only one of these compounds: salinomycin. It's noteworthy that the authors state that upon further retesting of the libraries, more compounds exhibited EMT-specific toxicity, thus suggesting that more thorough screenings using different compound libraries should be done.

Notably, salinomycin treatment indeed decreased the CSC subpopulation (defined as CD44^high/CD24^low cells) within breast cancer cells, while paclitaxel (a commonly used chemotherapeutic drug) treatment led to an enrichment of these cells, thus showing that in their system, the use of conventional chemotherapy can only effectively target the bulk of the tumoral population.

If these results hold true, it could mean that current therapies are effectively targeting the non-CSC population, thus slowing the tumoral progression, however not stopping it in the long run (it’s widely known that cancer recurrance is one of the major issues in cancer treatment). This relapse could be due to the enrichment of CSCs led to by conventional therapies. It is then possible that the use of selective inhibitors of CSCs as therapeutical adjuvants could then lead to better treatments (i.e. a combination of paclitaxel and salinomycin for breast cancer, for example).

It still remains to be seen whether the findings shown in this study are applicable in clinical settings, which takes me to the caveats of this paper: my main criticism regards the lack of validation in human samples. Every single experiment, (which as everyone knows in a Cell paper means a lot of data) is done with cell lines. The authors could have exploited their findings to analyze how xenografts of human breast tumors behave when mice are treated with the drug, for example. Furthermore, they could have analyzed if spontaneously generated breast tumors (such as the MMTV-PyMT model) respond to salinomycin alone or in combination with paclitaxel. Both the use of primary human breast tumors and spontaneous models of breast cancer would give much more insight into the potential of this compound in targeting CSCs in vivo.

The authors conclude:

“The importance of targeting CSCs derives from the multiple observations showing that CSCs, in addition to having increased tumor-seeding potential, are resistant to a variety of chemotherapy drugs and radiation treatment. As is shown here and elsewhere (Fillmore and Kuperwasser, 2008), treatment with paclitaxel actually imposes a strong selection for CSC survival and expansion. This suggests that in cases where chemotherapy or radiation treatment fail to completely eradicate the disease, the residual cancer cells will be highly enriched for cells that persist in a CSC/mesenchymal state. This notion is supported by recent clinical observations showing that after conventional chemotherapy, breast tumors have an increased proportion of cells with a CD44hi/CD24lo marker profile and increased tumorsphere- forming ability (Li et al., 2008). Collectively, these considerations indicate that to be effective in the long-term, cancer therapies should include agents that target CSCs to prevent the regrowth of neoplastic cell populations”

The field of CSCs is moving quite fast these days and exciting new findings are being published regularly. To conclude this post I just want to give a word of caution to most people outside the field (or even misinformed people in the field), regarding the conclusions that can be drawn from all the research being done. Only time will tell if the CSC hypothesis holds true for all or certain types of tumors and whether if this has any clinical relevance. Despite this warning and all of the issues raised, these are very interesting times to be involved in biomedicine.

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Gupta, P., Onder, T., Jiang, G., Tao, K., Kuperwasser, C., Weinberg, R., & Lander, E. (2009). Identification of Selective Inhibitors of Cancer Stem Cells by High-Throughput Screening Cell, 138 (4), 645-659 DOI: 10.1016/j.cell.2009.06.034

MANI, S., GUO, W., LIAO, M., EATON, E., AYYANAN, A., ZHOU, A., BROOKS, M., REINHARD, F., ZHANG, C., & SHIPITSIN, M. (2008). The Epithelial-Mesenchymal Transition Generates Cells with Properties of Stem Cells Cell, 133 (4), 704-715 DOI: 10.1016/j.cell.2008.03.027

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Quick post: Gurdon and Yamanaka win Lasker

The 2009 Albert Lasker Basic Medical Research Award, honored John Gurdon and Shinya Yamanaka

for discoveries concerning nuclear reprogramming, the process that instructs specialized adult cells to form early stem cells — creating the potential to become any type of mature cell for experimental or therapeutic purposes.

More here (Lasker Foundation) and here (news coverage, Bloomberg.com).

Here's a quote from the second link that's worth noting:

The awards include a cash prize of $250,000 for each category and often preview the Nobel Prize. In the 63-year history of the Lasker prizes, 76 winners also have won a Nobel.

[Images from Lasker Foundation]

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Good bye track I papers: PNAS

There are several ways to get your paper into PNAS (see ¹), which, IMHO, is a great journal.

One of these is the so called "track I" system:

Members are allowed to “communicate” up to two papers each per annum for non-members in their own sphere of expertise via Track I, for which the member procures at least two reviews before submission to the editorial office

Basically, what this means is the following: You (a non-member) send your manuscript directly to a member (i.e not going through the PNAS editorial office). The NAS member then sends it out for review (to whomever he chooses) and, after getting back their reviews, gets them to the PNAS editorial office with a recommendation.

Or, as PNAS puts it:

Before submission to PNAS, the member obtains reviews of the paper from at least 2 qualified referees, each from a different institution and not from the authors' or member's institutions. Referees should be asked to evaluate revised manuscripts to ensure that their concerns have been adequately addressed. The names and contact information, including e-mails, of referees who reviewed the paper, along with the reviews and the authors' response, must be included. Reviews must be submitted on the PNAS review form, and the identity of the referees must not be revealed to the authors. The member must include a brief statement endorsing publication in PNAS along with all of the referee reports received for each round of review. Members should follow National Science Foundation (NSF) guidelines to avoid conflict of interest between referees and authors (see Section iii). Members must verify that referees are free of conflicts of interest, or must disclose any conflicts and explain their choice of referees. These papers are published as “Communicated by" the responsible editor.

The other track, Track II, means submitting your work directly to the PNAS editorial office, where it will follow pretty standard MS handling.

As of 1 July next year, PNAS will force all non-members to submit to the journal directly for blind peer review, that is, through Track II².

Interestingly, over 80% of the Academy Members voted to eliminate Track I, although PNAS Editor-in-chief Randy Schekman mentioned that a “determined minority” opposed the move because they felt the option offered a publication route for innovative and idiosyncratic papers².

I don't have a particular problem with track I papers, but I've heard some people say (both here and in the US, about different papers): "the only reason he got this paper accepted in PNAS is because he submitted it through track I", or making comments about this track leading to a sort of "lite peer review" which could ease the way for a paper, as long as you have a "friend" as a NAS member to send your MS to.

I don't know if this is true, as I don't have any close experience with PNAS.

Does track I have a bad rep? Was this the reason why its elimination was so supported?
What do you think?

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¹ Fersht A (2005) How and why to publish in PNAS. Proc Natl Acad Sci U S A.102(18): 6241–6242.
²The Academy's Journal Becomes Less Friendly to the Academy Members

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The multifaceted p53, human mutation rates and more in my MolBio picks of the week from RB

Another week has gone by and some very interesting molbio blog posts have been aggregated into Researchblogging.org. Every week [see my inaugural post on the matter], I'll select some blog posts I consider particularly interesting in the field of molecular biology [see here to get a sense of the criteria that will be used], briefly describe them and list them here for you to check out.

This week, I selected 3 blog posts (4 actually, you'll see).

1) This year commemorates the 30th anniversary of the discovery of p53 and the 20th anniversary of its characterization as a tumor suppressor. As you may know, mutations in p53 (particularly in its DNA-binding domain) or alterations in its regulatory network are present in more that half of cancer cases.

p53 functions as a transcription factor and it regulates a wide array of genes in several stress response pathways, however some of its tumor-suppressor effects may be mediated in a transcription-independent way.

Charles Daney at Science and Reason comments on a study revealing one of these transcription-independent effects: p53 appears to enhance the post-transcriptional processing of a series of miRNAs with growth-suppressor functions, by direct interaction with the miRNA biogenesis machinery.

2) In two separate posts, David at the Atavism and Larry Moran over at Sandwalk (who actually published his post last week), discuss a recent article measuring the human Y chromosome base-substitution mutation rate by resequencing it completely (yes, completely using Illumina technology) from two men separated by 13 generations.
The authors arrive at a mutation rate of 3 x 10^-8 changes per nucleotide per generation, which is not so different from the error rate of DNA replication. This has nice evolutionary implications discussed at these posts.

3) Induced pluripotent stem cells (or iPS cells, linage-specific cells reprogrammed to a pluripotent state by the overexpression of certain transcription factors) are a hot topic right now.
Jacob Aron at Just a Theory highlights a PNAS article reporting a new method: the generation of iPS cells from adult human adipose stem cells (hASCs). Interestingly, iPS cells can be derived from this tissue without requiring feeder cells. Further, hASCs can be isolated in large quantities and are easy to maintain in culture.

That’s it for this week. Stay tuned for more MolBio Research Highlights!

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Some of the articles discussed in this week's selected posts:

Suzuki, H., Yamagata, K., Sugimoto, K., Iwamoto, T., Kato, S., & Miyazono, K. (2009). Modulation of microRNA processing by p53 Nature, 460 (7254), 529-533 DOI: 10.1038/nature08199

Xue, Y., Wang, Q., Long, Q., Ng, B., Swerdlow, H., Burton, J., Skuce, C., Taylor, R., Abdellah, Z., & Zhao, Y. (2009). Human Y Chromosome Base-Substitution Mutation Rate Measured by Direct Sequencing in a Deep-Rooting Pedigree Current Biology DOI: 10.1016/j.cub.2009.07.032

Sun, N., Panetta, N., Gupta, D., Wilson, K., Lee, A., Jia, F., Hu, S., Cherry, A., Robbins, R., Longaker, M., & Wu, J. (2009). Feeder-free derivation of induced pluripotent stem cells from adult human adipose stem cells Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0908450106

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How Science reporting works

[Thank to T. Ryan Gregory]

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Cell Press: Enhanced SnapShot

As you know, we at MolBio Research Highlights think that Cell Press rules (see The Scientific article of the future, Another one from Cell Press: free symposia! and More on Science 2.0: Cell Press).

We've talked about a feature called SnapShot before (handy one-page reference guides for important topics in cell and molecular biology, see here) and now Cell Press delights us with an upgrade: Enhanced SnapShot.

Enhanced SnapShots include features only possible online—animations, embedded captions, and dynamic visuals—all accessible by the click of a mouse. The goal of an Enhanced SnapShot is to provide everything currently available with the print SnapShot plus additional layers of information that are accessible through an easy to navigate webpage.

You can check some of the capabilities of this new format here.

Making full use of the capabilities of the internet in SnapShots, comes in line with the idea behind another Cell Press idea: the Article of the Future, which we've discussed before.

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Viral reassortment, genome transplantation and more in my picks of the week from RB

Another week has gone by and some very interesting blog posts have been aggregated into Researchblogging.org. Every week [see my opening post on the matter], I'll select some blog posts I consider particularly interesting in the field of molecular biology [see here to get a sense of the criteria that will be used] and list them here for you to check out.

This week, three blog posts made the cut:

1) Reassortment is a phenomenon in which genome segments of different viruses (with segmented genomes) infecting a single cell, can mix and lead to a viral particle containing segments of different origins, i.e with a new viral genome.
For this to happen, you need an individual infected by various viral strains (that is, a mixed infection), in which the reassortment can take place.

"Reassortment, notoriously, can generate rapid large changes in the personality of the virus. Pandemic influenzas have been reassortants, unrecognized by the population’s immune systems".

Ian York from Mystery Rays from Outer Space, discusses a recent article looking for evidence of mixed infection in humans, a necessary precursor to reassortment, from a collection of over 1000 influenza samples.

By using high-throughput sequencing, the authors show that ~0.5% of their samples — half a dozen individuals — were potentially mixed infections. Ian nicely discusses the implications of this and gives a nice summary of the results.

2) Daniel Ocampo-Daza at Ego sum Daniel comments on a recent article reporting a method to clone a Mycoplasma mycoides genome in yeast and then transplant it into a related species, Mycoplasma capricolum, producing viable colonies of M. mycoides (yes... Craig Venter is listed as an author). Daniel briefly comments on the methodology used and on the media hype these sorts of projects generate.

3) Respectful Insolence brings us an interesting and very critical post on a recent PNAS article describing a miRNA-mediated negative autoregulatory feedback loop in the estrogen receptor-α-dependent pathway, a pathway particularly important in breast cancer.

The following headline appeared in The Telegraph regarding this paper, a few days ago:

“Scientists two years from developing 'potential cure' for breast cancer”

Surely you realize how silly this is.

Orac speaks very strongly about the irresponsible and overblown media coverage the article has received (partly attributable to one of the authors?) and critically discusses some of the results, in light of these reports.

That's it for this week. Stay tuned for more MolBio Research Highlights!

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Some of the articles discussed in this week's selected posts:

Ghedin, E., Fitch, A., Boyne, A., Griesemer, S., DePasse, J., Bera, J., Zhang, X., Halpin, R., Smit, M., Jennings, L., St. George, K., Holmes, E., & Spiro, D. (2009). Mixed Infection and the Genesis of Influenza Virus Diversity Journal of Virology, 83 (17), 8832-8841 DOI: 10.1128/JVI.00773-09

Lartigue, C., Vashee, S., Algire, M., Chuang, R., Benders, G., Ma, L., Noskov, V., Denisova, E., Gibson, D., Assad-Garcia, N., Alperovich, N., Thomas, D., Merryman, C., Hutchison, C., Smith, H., Venter, J., & Glass, J. (2009). Creating Bacterial Strains from Genomes That Have Been Cloned and Engineered in Yeast Science DOI: 10.1126/science.1173759

Castellano, L., Giamas, G., Jacob, J., Coombes, R., Lucchesi, W., Thiruchelvam, P., Barton, G., Jiao, L., Wait, R., Waxman, J., Hannon, G., & Stebbing, J. (2009). The estrogen receptor- -induced microRNA signature regulates itself and its transcriptional response Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0906947106

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