Next time you talk about a piss-warm beer...

Scicurious has a post up about - quite literally - piss beer. It describes a situation where yeast infections cause the fermentation of bodily fluids:

The second patient had “turbid” urine (that’s cloudy), and they suspected yeast, especially when they opened the bag of urine, and smelled BEER. Apparently this was so odd that the urine sample passed to every doctor in the room and down the hall. I can just picture a group of people in white coats, all gathered around with a cup of suspiciously yellow liquid, sniffing and saying “HEY GUYS! You gotta smell this!!!” Apparently the poor patient was so yeasty that her breath, and literally everything about her smelled like beer, and alcohol could actually be detected as a byproduct of the yeast.

(cue comparisons to your least favourite brew) I guess this is a bit of a different take on the human decanter.

Aneuploidy Hampers Yeast Cell Proliferation

We recently discussed on the bayblab whether gross chromosomal abnormalities such as aneuploidy, frequently observed in cancer cells, are cause or consequence of tumor formation. A new paper from Torres et al. shows that yeast with extra chromosomes actually grow slower, suggesting that the relationship between aneuploidy and cancer might be a bit more complex (if the phenomenon holds true on human cells). Then again, maybe yeast are just, well...yeast.

Hiding From the Noise - Essential Genes Cluster in Open Chromatin?

We've previously discussed on the bayblab how the same transgene can provoke different murine phenotypes depending on which genomic locus it is expressed from. We've also discussed work demonstrating how noisy gene expression seems to be caused by stochastic bursts of mRNA transcription. A new paper in Nature Genetics ties together these ideas with the observation that essential genes tend to physically cluster within specific regions of genomes.

Based on the reasoning that transcriptional noise arises from the stochastic relaxation of otherwise closed chromatin, Batada and Hurst argue that essential eukaryotic genes tend to cluster within regions of open chromatin because these regions are relatively free from transcriptional noise. This would minimize the possibility of random fluctuations in expression that would kill the cell and therefore provide a selective advantage to those cells whose essential genes cluster together in less noisy regions. They present bioinformatic analyses of yeast data that seem to support this idea.

I like the idea, but am not totally sold on the notion of "essentialness". Yeast essential genes are based on those which are lethal when mutated in yeast grown under the warm and loving conditions of laboratory culture. However, the yeast genome did not evolve in the lab, it evolved in much harsher and variable natural environments. The the real set of essential genes is likely to be much larger than defined here, in fact it may include the whole genome as it is likely that each gene was essential at some point in yeast evolution. This said, even in natural environments, there maybe a spectrum of gene essential-ness, with some genes essential over a broader range of conditions, or longer evolutionary time-span than others. Thus the lab essential genes may actually reflect the core set of "most essential genes". But can we take this for granted?

Glow in the dark terrorists

A recent paper in Nature Chemical Biology (arm and leg subscription required) describes a engineered yeast strain engineered to sniff out TNT. First they had to clone many G protein signalling components into a yeast strain such that mammalian olfactory receptor signalling functioned. Then they screened a library of cDNAs from olfactory receptors to obtain a rat olfactory receptor that responds to TNT. This signaling pathway then initiated the expression of green fluorescent protein, thus the yeast glowed green when in the presence of trace amounts of TNT and an awesome biosensor is born. Great work from Dr. Danny Dhanasekaran at Temple University School of Medicine.

Mitochondrial Madness

Our often-neglected bacterial endosymbionts the mitochondria seem to have their fingers in all aspects of eukaryotic cell functioning. Not only do they make us ATP and tell our cells when to die, they even have their own genome, which they can replicate, transcribe and translate all on their own. But mitochondria don't just use proteins encoded in their own genomes; they've also got some out on loan from the nucleus. And this is where the madness begins. Somehow this excellent Molecular Cell review on mitochondrial transcription found its way onto my lab bench, so I read it. Here are a few of the mind-blowing facts you can discover therein:

• The eukaryotic single-subunit mitochondrial RNA polymerase was ganked from bacterial viruses (bacteriophage T3/T7), and has no relation to those encoded by bacteria themselves.

• Even weirder, the phage-like mtRNA polymerase is encoded in the nuclear genome of eukaryotes. Interstingly, an isoform of mtRNA polymerase lacking a mitochondrial localization signal performs transcription of nuclear-encoded genes in the nucleus (RNA pol IV).

• The amino-terminal domain of yeast mtRNA polymerase has diverged from its phage ancestry, and has evolved to mediate coupling between mitochondrial transcription and translation. In fact, mutations in the ATD lead to deficiencies in mitochondrially-encoded OXPHOS enzymes and thereby decrease lifespan in yeast.

• What? Mitochondrial translation? What's up with that? Nobody really knows...

Also, check out this wicked album of artistic renditions of cells by Gary Carlson which I ganked the above photo from. Nice job Gary!