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Mitos, in dark blue, dance aroundthe nucleus of a HeLa cell. Below,blue mitochondria comingle in thegreen cytoplasm of a rat liver cell.Mitochondria. It’s not going too far to saythat these energy-producing organelles—scatteredabout inside our cells and numberingup to thousands in each—are the reason we’rehere. Not just Van Houten and this reporter,but all of us and pretty much every otherliving thing that’s more advanced than a bacterium.One could write a book about theirevolution and purpose—British biochemistNick Lane did with 2005’s Power, Sex, Suicide:Mitochondria and the Meaning of Life. (Thetitle is not at all hyperbolic. Really.)The Dementedly Short Version in WhichDates and Occurrences Are Generally butNot Universally Agreed Upon: About 4.6 billionyears ago came the Earth. Then, about800,000 years later, life appeared on Earth inthe form of bacteria. Bacteria ruled for a long,long time. About 2.4 billion years ago, Earth’satmosphere became oxygenated. A billion orso years after that, an archaebacterium (whichcould live under extreme conditions such asthose found in geysers) without membraneencasedstructures developed a symbiotic relationshipwith a eubacterium (bacteria we aremore likely to come across today, which liveunder more conventional conditions). Theyeventually fused together and, more or less,became one. This “hopeful monster,” as Lanecalls it, became the first true eukaryote. Lots oftrue eukaryotes ganged up, diversified, specialized,and became the components of complexbeings, ranging from plants to humans. Andthat eubacterium that fused? Seems that ithelped create the mitochondrion and cellnucleus. Its own small genome stayed withthe mitochondrion, but it also shed many ofits original genes into the larger cell nucleus.It makes energy in the form of adenosine-5triphosphate (ATP). It persuades a cell to diein a quiet and peaceful way when the cell hasbecome damaged. The tiny little organelle hasbecome a big part of us.For us to thrive, mitochondria need tobehave themselves and work well, generatingthe energy our cells need to live. We’re in troublewhen mitos go bad. That can mean cancer,neurodegenerative diseases, devastatingendogenous mitochondrial DNA disorders,muscle wasting with age. Pitt investigatorsare part of a recent resurgence of interest inmitochondria, and they have a finger in everymitochondrial pie.Van Houten has long been a student ofDNA damage and repair in the cell’s nucleus,a field of study considered important to understandingaging and cancer. But throughout thepast decade or so, he has developed and actedon a hunch that the ability of the mitochondrionto repair its own DNA may be equallyfundamental to our health. Van Houtenbelieves that unrepaired insult or injury to themitochondria’s DNA (mtDNA) is the beginningof a nasty and self-perpetuating chain ofevents that may be responsible for the majorityof adult-onset diseases, including cancer.And work that began with a postdoc in hislab appears to reveal why many tumor cellscan be so tenacious (it has to do with theirfeeding habits) and could pay dividends in theform of a novel mitochondria-targeted cancertreatment.“The chemistry works,” he says of thisexperimental work. “We don’t know how, butthat’s okay. Nobody has ever shown this.”The buffalo bites come, and anotherbeer is ordered. Time to get down tobusiness. Van Houten, a PhD, theRichard M. Cyert Professor of MolecularOncology in Pitt’s Department ofPharmacology and Chemical Biology, was askedto think of a few promising mitoresearchersto be featured in this story. He opens a folder,pulls out two sheets of paper labeled “PittsburghMitochondriacs”—those who are maniacal formitochondria, of course. The list is 24 nameslong.Asking Van Houten to narrow down the listis fruitless. “He does great work!” “She does greatwork!” “Oh, he does great work, too!” “Her workis excellent!” He scribbles a few diagrams on thepages. An alphabet soup of proteins follows.Another “(insert name here) does great work!” Ashortened short list of Pitt research and researcherswe really should know about, according to VanHouten: A postdoc with a potential biomarkerfor Parkinson’s. A biochemist’s long-standingwork in mitochemistry. Mitos and the injury thatresults when blood supply is returned to oxygendeprivedtissue. An oncogene that actually controlsmitochondrial biogenesis. A new compoundthat protects mitochondria from radiation. Agingmice with signs of mitochondrial dysfunction.Mitos and exercise. Mitos and fruit flies. … VanHouten is infectiously enthusiastic about mostthings, but nothing more than science and thepeople, particularly those here at Pitt, who do it.Mitorelated research has become so fruitfulin recent times that last year Van Houten andLotze organized and executed the first RegionalTranslational Research in Mitochondria, Aging,and Disease Symposia. The second set of symposiais planned for Saturday, Oct. 20, at the UPMCCancer Pavilion. (For those who want to startstressing their mitochondria first thing, there’s anoptional 10K “fun run” at 6:30 a.m.)The buffalo bites are long gone, a plateof nachos has disappeared, and several pagesof notes later, the whirlwind introduction tomitochondria is over, for tonight anyway. Thiswriter’s head is swimming, not from the beerbut from mito info. So, with limited time andspace, we begin our journey to the center of themitochondria with Van Houten himself. (Thestories of some of the others Van Houten effusedover will be told in a future edition of the PittMitochronicles.)After earning his doctorate at the OakRidge Graduate School of BiomedicalSciences in Tennessee and completing afellowship at the University of North Carolina,Chapel Hill, Van Houten, in 1988, found himselfin New England, a young professor at theUniversity of Vermont. He had been hired to24 PITTMED