This paper was a bit of a family affair. As you can see above, I am the "first author" of this paper, but my wife also appears as a "middle author" (i.e. she had substantial scientific contributions to the paper- this was while she was working in my lab the year before entering graduate school).
[In case you missed it the first time]
Moreover, while he is not acknowledged in the paper, my brother Brian gave a helping hand as well. I needed to run a program in Linux, but the program was no longer being updated/supported, and thus the OS needed substantial modifications to run the program. Who better to ask than Brian Norris??
[The experiments marked in red- made possible in part by Brian Norris (from pages 950 and 957)]
And remember this picture, from when Mom came to visit and insisted on helping me with my experiment?
Well that happened to be a last-minute experiment for this paper (required by the reviewers). I was harvesting worms to measure their RNA levels by "RT-PCR," and she was helping me harvest them. Here are the results:
[Made possible in part my Sandra (Mom) Norris (from "supplemental data")]
So there you have it. Norris et al. 2014. With contributions by no less than four Norrises.
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Appendix:
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If, per chance, you would be interested in my attempted explanation of the research contained in this paper tailored to a lay audience, read on:
(1) Most genes in animals are modular, in that individual modules (called exons) are spliced together to form "mature RNAs" from which proteins are made. Think of it like a film- there's a ton of raw footage, from which a handful of modules (scenes) are spliced together to make a coherent film.
(2) Many of these genes can be spliced together in a multitude of ways, in a process called "alternative splicing". Individual exons can be included in some RNAs, whilst being excluded from otherwise identical RNAs from the same gene. Think of it like alternate cuts of a movie- director's cut, final cut, extended-special-edition cut, etc. They're all the same movie, but each is partially unique.
[Wikipedia image- a gene before splicing on the left, after splicing on the right. The bottom example would be analogous to the theatrical cut, and the upper analogous to the director's cut (because it has an extra "scene" included!)]
(3) Points (1) and (2) were already known before my paper. I endeavored to observe: how prevalent is alternative splicing between different types of neurons? In the analogy, the question would be- for most genes, do all neurons possess the same version of the film, or is there substantial use of alternative editions from one neuron to the next? The answer turned out to be the latter- alternative splicing within the nervous system is widespread and diverse.
(4) One particularly interesting case of alternative splicing was in a gene that was spliced in one way in excitatory motor neurons (the neurons that allow you to flex your muscles) and spliced differently in inhibitory motor neurons (those that allow you to relax your muscles). The rest of the paper seeks out the mechanism and identifies the "director" responsible for this alternative splicing event (it turns out to be two different directors! [i.e. two different proteins]).
(5) Why is this important? We think alternative splicing is critical for increasing the complexity of cells and complex organs like the brain. It may well be that complex organisms and/or nervous systems would be impossible without robust alternative splicing. Indeed, many neuromuscular diseases (as well as cancers) are associated with failures in proper splicing and/or alternative splicing. Therefore understanding its proper regulation is of high importance.
