The lab gloves came off in a recent Nature exchange on the putative role of the transcriptional repressor, REST, in embryonic stem cell pluripotency.
In the left corner, Singh and colleagues, conducting experiments out of MD Anderson in the Lone Star State, published data in Nature back in May, 2008 indicating that REST may control the self-renewal and pluripotency of ESCs by suppressing miR-21 after experiments disrupting a REST allele resulted in lower expression of several pluripotency related genes. Last week in Nature, Singh’s work took a few jabs.
Jorgensen and colleagues working out of Imperial College in London, countered these earlier findings with data suggesting that knocking REST partially, or even completely, does not impact ESC potential as measured by the gene expression markers. Buckley and colleagues at King’s College in London, chimed in on things as well, supporting Jorgensen’s data, while adding in various ChIP data sets suggesting no such regulation of miR-21 by REST.
Both groups cited previous findings that supported their data, making a compelling story for each.
But, Team Singh fired back, citing a number of findings supporting their suggested role of REST and miR-21 in self-renewal and pluripotency. They also offered a very interesting, potential explanation for the labs differences…cell culture.
That’s right Singh suggests that the Jorgensen experiments used feeder cells in most of their experiments, which according to Singh, “dampens the requirement of REST-mediated maintenance of mESC self renewal and pluripotency.”
Team Singh also countered on the Buckley data, suggesting that their use of higher passage cells could be the reason for the discrepancy. This one was too close for us to call, but you can catch all the highlights in Nature, Feb 2009