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MolBiol Carnival #18!


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Welcome to the (ever so slightly late — sorry) 18th issue of the MolBio carnival!

[insert some awful pun involving strains here]

For those of us working with live cultures, it’s important to remember they have a pedigree, and ultimately come from somewhere outside the lab (after all, all life has a common ancestor somewhere…). Sometimes the source can be interesting, sometimes even of immediate relevance to research. Sometimes searching for the source of your cultures can lead you to risk getting shot while trespassing in rural, Confederate-flag-studded, southern Indiana farmland looking for ponds your Paramecium strains were isolated from, 80+ years ago (going that way would prob earn me a somewhat awesome obit in a protistology journal somewhere…). Of course, this is all trivial compared to the complexity surrounding origins of mammalian cell cultures, particularly those conspecific to us. At Reportergene 96well wonders Where are your cells from?

Continuing on with our theme of strain origins and selection, Connor Bamford at Rule of 6ix ponders the effects of strain choice on research results. I’ve often wondered how truly typical a (protist) type strain can be, particularly in cases where a critter’s been isolated only once. Is it normal? How much does the ‘species’ vary, anyway? What if we got a total freak by accident and now paint the rest of its kin with a tainted brush? This is also a problem in the world of pathogenic microbiology (apparently some microbes have something to do with disease…and people study them to kill them), particularly as one attempts to study human diseases through infections of insanely-closely-related-but-still-not-the-same rodents and monkeys. Furthermore, these strains (both pathogenic and harmless-yet-really-cool-so-fund-us-NIH/CIHR-dammit) have histories, particularly what has happened to them after capture and domestication in the lab. This modifies the organisms* in ways that can later screw with research. Read more in Certain strains put a strain on virus research.

* A fundamental change in their lives is the drastic bottlenecking (reduction in effective population size) that a microbial strain experiences upon capture and cultivation — every time you pick a colony and streak it out, you bottleneck the poor guys to a population of 1 (one!) — do this routinely, and you’ve just unintentionally done one of my painful ‘paid hobbies’ at the moment: mutation accumulation experiments. One can only wonder how many nasty-but-tolerated deleterious mutations have been picked up by celebrity lab strains…

[I had a transposon-related pun here but it jumped away =(]

In On Transposable Elements and Regulatory Evolution at biobabel, Habib Maroon discusses the exaptation of transposons as regulatory elements ensuring some genes are transcribed at the right time and place. Some authors have even termed this ‘domestication’ — do keep in mind, however, that this didn’t come about by the organism sitting there thinking “hmmm, perhaps I should put these transposons to good use”, but probably rather through initially fortuitous protein-transposon segment binding that later became depended upon and largely irreversible. Rather than cheap adaptationist explanations, this makes the question of the evolutionary mechanisms of this transposon ‘domestication’ all the more fascinating, and I hope some people are/will be looking into this!

DMD, reportedly the longest gene known, is a cytoskeletal linker gene involved in muscles. Its length renders it a massive mutational target, some defects leading to muscular dystrophy, for example. Among the nastier mutations are insertions or deletions leading to frameshifts capable of resulting in random stop codons where there shouldn’t be any, effectively terminating the protein early. Turns out, you can introduce single stranded RNAs to fix these frameshift mutations, in an interesting case of gene therapy explained by EE Giorgi at Introns, exons, and stop codons: how antisense oligonucleotides can fix frameshift mutations at CHIMERAS.

Aphids reproduce mainly parthenogenically (that is, asexually, in females), leading one to expect all the offspring to be clonal (genetically identical to each other). Amazingly, the offspring vary quite a bit in shape, colour, pathogens — you name it. Furthermore, they vary in chromosome numbers! Further reading reveals that aphid chromosomes are just weird, but I won’t spoil it for you — go read Stability of instability? when karyotype is never the same at The aphid room by Mauro Mandrioli

[You're really gonna have to upgrade your browser to see the tiny bacteria here]

At Memoirs of a Defective Brain, Defective Brain itself(! apparently feebly tenticulated too) writes about The Beetle to Beat TB discussing glowey genes in bacteria, with truly wonderful illustrations! At the beginning we learn this little tidbit: apparently there’s a bacterial pathogen that devours caterpillars and makes their carcass glow, attracting nematodes which the bacteria then devour too. That’s freaking awesome. Then we learn that more does not necessarily mean better (it’s what you do with it that counts — more can lead to faster exhaustion). There’s an important point those of us who’ve played with transgenic awesomesauce should all think about: different tRNAs can be popular in different species, meaning you can have your pet gene expressed in metric craptons but largely ignored by the translational machinery. In short, despite all the defectiveness, this is a great description of the work that goes into making all sorts of fancy glowey genes work in foreign organisms.

And last, but very definitely not least, we have ‘just’ another wonderful post by S. E. Gould (Lab Rat here at SciAm) explains How bacteria sneak into your blood through your mouth — also with fun illustrations! While our body (and immune system therein) struggles to maintain a “bacteria-free zone”, some sneaky bastards have figured out ways to make holes in our defenses and creep in anyway — though the mouth, even! Fusobacterium nucleatum has a nifty little protein that happens to bind a cell surface protein that glues our cells together, eroding it away, and the rest is history. Not all bacteria have this, and a question that you have to read the post to answer is whether other bacteria can also slither in following Fusobacterium‘s vandalism of your mouth.

 

That’s it, hope y’all had a good time. Next round of MolBiol goodness will be at… unknown (I’m guessing that could be you!). Please submit any awesome posts pertaining to molecular biology, yours or otherwise, using this carnival submission form. With such vast swaths of biology and medicine involving some form of molecular biol, we should really be kicking ass in having an ocean of submissions and content! ;-) If you’re an attention-deficient blogger (like me), carnivals are a great way to be forced to actually read a few blog posts!

Psi Wavefunction About the Author: Psi Wavefunction is a graduate of the University of British Columbia working as a protist researcher (soon to be graduate student) at Dalhousie University in Halifax, Nova Scotia, and blogs about protists and evolution at The Ocelloid as well as at Skeptic Wonder. Follow on Twitter @Ocelloid.

The views expressed are those of the author and are not necessarily those of Scientific American.





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