PROVIDENCE, R.I. [Brown University] Diseases from a mutation in one genome are complicated enough, but some illnesses arise from errant interactions between two genomes: the DNA in the nucleus and in the mitochondria. Scientists want to know more about how such genomic disconnects cause disease. In a step in that direction, scientists at Brown University and Indiana University have traced one such incompatibility in fruit flies down to the level of individual nucleotide mutations and describe how the genetic double whammy makes the flies sick.
"This has relevance to human disease but it's also relevant to all organisms because these two genomes are in all animals and all plants," said David Rand professor of biology at Brown and senior author of the study published online Jan. 31 in PLOS Genetics. "There are a lot of metabolic diseases that are mitochondrial in origin and they have peculiar genetic tracking a two-part system needs to be considered."
Five years ago at Brown, Rand and two postdoctoral researchers Colin Meiklejohn, of Brown and Indiana University, and Kristi Montooth, now an assistant professor at Indiana University began searching for an example in the convenient testbed of fruit flies. They started mixing and matching mitochondrial and nuclear genomes from different strains and species of flies that carried natural mutations produced during evolution to observe what conflicts might arise. They found that when they placed the "simw 501" mitochondrial DNA from Drosophila simulans flies into Drosophila melanogaster flies with "Oregon R" nuclear DNA, bad things happened.
The flies with this combination lived but had an array of problems. Their most noticeable flaw was that whisker-like bristles on their backs were only half the length of those in normal flies. The flies also had developmental delays, reproduced less effectively, and tired more quickly, which makes sense because the mitochondria is the cell's
|Contact: David Orenstein|