Almost* all mRNAs in a eukaryotic cell have a poly(A) tail that is added by a conserved complex of proteins. Given that the poly(A) tail is added by a processing event, the question arises as to how this complex knows when and where to process the mRNA. The answer, to a first approximation, is that polyadenylation is guided by specific sequence signals carried by the precursor mRNA itself – the so-called polyadenylation signal. Read the rest of this entry »
Recently, we learned of an instance of the de novo origination of a new protein-coding gene in yeasts. This instance involved a mechanism or pathway that seems difficult to some, namely the random appearance of an open reading frame in an otherwise noncoding segment of DNA via judicious appearance of translation start and stop codons. The question naturally arises as to the relevance of such a pathway to real-life biology; was/is this a rather rare event that doesn’t really contribute to protein evolution, or is it a common means by which the protein-coding capacity of a genome is augmented?
A paper that is in press in Genome Research (Zhou et al., “On the origin of new genes in Drosophila”) gives us some insight into this question. The abstract of this paper summarizes things as well as I can:
File this under the “About me – proud father” category. Last summer, Professor Steve Steve had a special escort during his visit to the Creation Museum in Northern Kentucky. This escort is an author of the first essay in this anthology (see also this site). This morning, she had an essay posted on The Huffington Post. It’s about first-time voters and the up-coming election.
What’s this got to do with this blog? Well, in case you haven’t figured it out, I’m talking about my youngest daughter, Amy Hunt. If you want to read some good stuff (even if it isn’t science), check out her essays. Professor Steve Steve has… Read the rest of this entry »
That’s how long it’s been.
The NBA championship is back where it belongs.
OK, so I’m not on the Scienceblogs roll, but the question is still a good one …
Asked here: “Why do you blog, and how does blogging help with your research?”
My answer to the first question is because I love to talk about science. And I also like to hear myself talk, and think. It’s really that simple.
The answer to the second question is most definitely. At several levels. For example, it is pretty easy to forget how to communicate with those who are not as deeply buried in their work as scientists tend to be. Blogging broadens the audience, and teaches me to say things in ways that others, especially somewhat educated people who are not intimately familiar with a subject, can understand. This is a very important skill – if I can get a complicated point across to a blog audience, I feel I have a good chance of getting the same point across to, say, a grant panel that does not include an expert in my particular field. When one recalls that members of the panel have to struggle with 10-30 grants over the course of 3 weeks or so, AND they are subsequently cooped up in a room for a couple of days, spending at most 10 minutes on a proposal, one can appreciate how clear and concise writing is important.
Ditto for reviewers of papers. (Then there’s the matter of the “lay language summary” – stay tuned for a new category that I am plotting for later this summer.)
For me personally, my blogging (and, before blogging caught on, participation on discussion boards) has helped my research in very tangible ways. The best example I can think of – I worked up the nerve to develop and propose a rather risky and unconventional approach to our studies of polyadenylation factors for an NSF proposal partly as a result of much discussion on some ID boards (of all places). Beyond the fact that the proposal was funded, the approach developed many fascinating leads that my lab will be pursuing for years to come, and already one small peer-reviewed research paper. There are other benefits, but this is the one that comes immediately to mind. If asked, I’d be glad to elaborate in the comments.
I hope that helps.
A recurrent theme amongst ID proponents is the supposed difficulty of protein evolution, especially as it relates to the origination of new protein-coding genes. This is, I suspect, a key reason why ID proponents such as Paul Nelson are so enamoured of ORFans, and a foundational principle for the application of ID theory to evolution (the idea being that protein-coding genes are possessed of Complex Specified Information, and thus cannot arise by natural processes). Thus, studies that pertain to the origins of new protein-coding genes are going to factor largely in the scientific aspect of the ID debate, especially since ID proponents insist that new protein-coding genes cannot arise “by chance”.
It is in this context that a recent study by Jing Cai and colleagues is of interest. The title of the article suffices to explain the study – “De novo Origination of a New Protein-Coding Gene in Saccharomyces cerevisiae”. What these authors describe is a series of studies of a yeast gene, BSC4. This gene was originally identified as a candidate containing a so-called read-through translation termination (or stop) codon. This gene was studied in more depth, whereupon Cai et al. found that the protein encoded by this gene was novel in genome databases, not resembling any other protein in any organism. Importantly, this includes the genomes of related Saccharomyces species; this indicates that this protein in S. cerevisiae arose relatively recently, after this species diverged from its close relatives.
Just a note of explanation for those who pay attention to the Category labels. An occasional occurrence on this blog will be essays that pertain to Intelligent Design. Some of these will be re-posts of essays I have contributed to The Panda’s Thumb and to older discussion forums (such as the ARN and ISCID boards). Others will be newer contributions that will be cross-posted to The Panda’s Thumb. I do this for a number of reasons. This practice is homage in a way to the hobby that got me into the blogging business. It’s also acknowledgement that this hobby has caused me to become more knowledgeable about many subjects that have little to do with RNA. This has translated into some bona-fide research and discovery.
So enjoy the essays in this category.
I’m not sure how often I will do this, but I thought I would point out a paper I have co-authored with scientists at the University of Massachusetts Lowell and Miami University in Oxford OH. The brief bottom line is that a plant polyadenylation factor subunit may be involved in regulating gene expression in response to oxidative stress.
This is my first foray into PLoS One, and I’m interested in seeing how one may generate feedback and discussion. The abstract follows. Enjoy.
In biology, genetics, biochemistry, and molecular biology classes, one of the things that we used to learn that distinguishes prokaryotes from eukaryotes is the “fact” that eukaryotes have polyadenylated mRNAs, while prokaryotes do not. This morphed rather easily into a distinction – eukaryotes do polyadenylation, prokaryotes do not. For years, this was standard fare in class. However, even as generations of students (beginning with the discovery of polyadenylate tracts in hnRNA in eukaryotes) were learning of this distinction, we knew that all was not right with this. Among the lurking pieces of conflicting data was that the first biochemical entity that was shown to add poly(A) tracts to RNAs in vitro was a bacterial one, isolated and purified from E. coli (1).
Previously, I summarized the importance of the poly(A) tail of mRNAs. As I stated in that essay (and as one can tell by perusing the background stuff and some of the links here), what I am interested in is how the poly(A) tail is actually added to a mRNA. The point of this essay is to provide an overview of what we know, so that future essays on the subject may have a better context. I’ll structure this essay as a series of bullets (ideally, they’d be concise, but knowing me that’s not too likely).
Read the rest of this entry »