Back in 2002, one could read in the New York Times,
An analysis of the mouse genome by an international consortium of scientists, a landmark event in biology, shows it is so similar to that of people that it should speed efforts to understand the human genome and the genetic roots of disease.
This is the first time that the reasonably complete genomes of two mammals, mouse and man, have become available for comparison. While the genome of a mammal even closer to the human, like the chimpanzee, may someday be decoded, the mouse is both genetically close and also an ideal laboratory animal.
Man and mouse are cousins, each descended from a small mammal that split into two species toward the end of the dinosaur era. Despite 75 million years of separate evolution, only about 300 genes — 1 percent of the 30,000 possessed by the mouse — have no obvious counterpart in the human genome, according to the new analysis published in today’s issue of Nature.
A friend writes to clarify,
99% of mouse genes have a homologue does not mean that they are 99% similar. It means for 99% of human proteins, the mouse has the same protein but with a slightly different sequence.
Meanwhile, chimp lab research ended in 2011, due to lack of necessity.
And now this. From ScienceDaily:
Looking across evolutionary time and the genomic landscapes of humans and mice, an international group of researchers has found powerful clues to why certain processes and systems in the mouse — such as the immune system, metabolism and stress response — are so different from those in people. Building on years of mouse and gene regulation studies, they have developed a resource that can help scientists better understand how similarities and differences between mice and humans are written in their genomes.
Their findings — reported by the mouse ENCODE Consortium online Nov. 19, 2014 (and in print Nov. 20) in four papers in Nature and in several other publications — examine the genetic and biochemical programs involved in regulating mouse and human genomes. The scientists found that, in general, the systems that are used to control gene activity have many similarities in mice and humans, and have been conserved, or continued, through evolutionary time.
The results may offer insights into gene regulation and other systems important to mammalian biology. They also provide new information to determine when the mouse is an appropriate model to study human biology and disease, and may help to explain some of its limitations.
Limitations? So the genome is not a Lego set?
From The Scientist’s take:
Mice are widely used to model human metabolism, disease, and drug response. But results published today (November 17) in PNAS reveal widespread differences between human and mouse gene expression, both in protein-coding and noncoding genes, suggesting that understanding these disparities could help explain fundamental differences in the two species’ physiology.
Mice are widely used to model human metabolism, disease, and drug response. But results published today (November 17) in PNAS reveal widespread differences between human and mouse gene expression, both in protein-coding and noncoding genes, suggesting that understanding these disparities could help explain fundamental differences in the two species’ physiology.
Michael Snyder of Stanford University and his colleagues compared how genes are expressed in 15 different human and mouse tissues, including brain, heart, liver, and kidney. They found that gene expression patterns clustered by species rather than tissues. For example, gene expression in a mouse liver more closely resembled the patterns observed in a mouse heart than those observed in a human liver. Using data from the ENCODE and modENCODE projects, among other sources, the analysis spanned “the most tissue-diverse RNA-seq dataset to date,” the authors wrote in their paper.
Advancing knowledge is always a good thing.
But it is fair to say that the purpose of lab work with mice was not to elucidate disparities between their genome and ours. That is a subject in which taxpaying stakeholders have no more intrinsic interest than they would in the disparities between the genomes of pigs and humans. Some things we just take for granted for free.
This must impact the perceived usefulness of mouse models, as The Scientist acknowledges:
These data “guide us as to where a mouse model might be useful and where to be more cautious,” said Snyder. “A mouse and human have almost the same genes. But how we express those genes differs quite a bit.”
We will watch developments with interest.
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