Thank you for the great ISSCR talk coverage, Eva Amsen and Seema Grewal! I very much enjoyed ISSCR this year, and thought I’d chime in with a little talk coverage too (especially of the first day that you were unfortunately unable to attend). But first, I’ll give a little background on myself, since I have not posted here before. My name’s Teisha Rowland and I am a PhD graduate student at the University of California in Santa Barbara, where I do research with human embryonic stem cells (hESCs) and induced pluripotent stem cells (iPSCs). I am also a science writer and maintain a blog on stem cells called “All Things Stem Cell” (http://www.AllThingsStemCell.com) and I also have a weekly biology column with the Santa Barbara Independent called “Biology Bytes” (http://www.independent.com/bio) (about one third of my articles are on stem cells). Before the talks started Wednesday afternoon, ISSCR highlighted their new website for people considering stem cell therapies. Whether you’re considering a therapy or not, their new website, “A Closer Look at Stem Cell Treatments” (http://www.closerlookatstemcells.org), is definitely worth checking out. The importance of using the right language when communicating with the public, and only saying what can actually be done with the current technology, was emphasized. Shinya Yamanaka discussed making human iPSCs using the reprogramming factor L-myc instead of c-myc. C-myc (along with Sox-2, Oct-4, and Klf4) was originally used by Yamanaka’s group to reprogram adult cells to become iPSCs (c-myc promotes reprogramming efficiency), but activation of c-myc has also been linked to tumor formation. Consequently, Yamanaka’s group tried reprogramming cells using L-myc instead of c-myc. L-myc is not found in cancers, but has a weaker transfection rate. However, by using L-myc instead of c-myc it was found that more iPSC colonies (and fewer non-iPSC colonies) were created (than with c-myc). Lastly, Yamanaka touched upon the importance of creating large iPSC banks for disease treatments, but that in order to do this researchers must decide on the best cell origins to use and the best reprogramming technique. Marius Wernig then gave a talk on a recently published paper by his group on direct reprogramming, a topic that will surely only get more research attention in the future. Wernig’s group took fibroblasts from the tails of mice and directly reprogrammed them into functional neurons (http://www.nature.com/nature/journal/v463/n7284/full/nature08797.html). They initially screened 19 candidate factors and were able to narrow it down to 3 (Ascl1, Brn2, and Myt1l). (Back in February, I actually wrote an article on the amazing topic of direct reprogramming, with coverage of Wernig’s findings – for those of you who are interested, it can be found at http://www.independent.com/news/2010/feb/20/direct-reprogramming/ .) K. Lenhard Rudolph gave an interesting talk on stem cells, telomeres, and aging (http://www.springerlink.com/content/k462767001824386/). Stem cell function is known to decline with age, and Rudolph’s group has found this to be a response to telomere dysfunction. He showed that mice with dysfunctional telomeres display premature aging (from studies in knock-out mice) and have impaired tissue regeneration, a function that stem cells play a central role in. In his talk, Jamie Thomson suggested a bit of a change in how stem cell researchers think of hESCs and their pluripotency. hESCs are pluripotent (they can ultimately become nearly any cell type), but Thomson explained this is done through a step-wise process; hESCs give rise to some progenitors, which give rise to more mature cell types, which eventually differentiate into the target cell type. Thomson brought up an interesting question -- Is this final hESC differentiation step similar to adult/somatic stem cell differentiation, and hESCs are just able to initially become a wider array of progenitors? If this is the case, it’s quite important to understand hESCs’ early lineage choices. This early differentiation time point is still very unclear; as Thomson points out, hESCs can differentiate into trophoblast cells (http://www.nature.com/nbt/journal/v20/n12/abs/nbt761.html), which “makes no sense” (trophoblast cells are from the outer layer of the blastocyst, while hESCs are isolated from the inner cell mass). Thomson suggested that FGF plays a key role in this early differentiation point; high levels of FGF can block trophoblast differentiation, and FGF can also direct hESC differentiation to the primitive streak. With growing interest in chromatin remodeling during reprogramming to create iPSCs, Kathrin Plath’s talk was quite timely. Plath explained that pluripotency is related to having two active X chromosomes, and that a somatically silent X chromosome is actually reactivated during reprogramming (http://dev.biologists.org/content/136/4/509.abstract). (Interestingly, the reactivated X chromosome can easily be silenced again due to oxidative stress or just expansion in culture.) So, how is the X chromosome reactivated during reprogramming? Plath’s group found that during reprogramming the normal pluripotency genes are activated, and changes to the chromatin structure occur, all prior to the reactivation of the X chromosome. Consequently, further investigation of changes to chromatin structure during reprogramming should greatly help clarify what it means to be pluripotent. Lastly, Grigori N. Enikolopov presented data that help solve the mystery of where neural stem cells disappear to as a person ages. It’s known that the number of hippocampal neural stem cells (and consequently neurogenesis) declines with age, but how or why this happens has been unclear. Enikolopov’s group found that these cells don’t just vanish; they turn into astrocytes. And the stem cells do so through asymmetric visions (unlike other adult stem cells), meaning that once they become “active” they leave no stem cell replacement behind. Consequently, as a person ages Enikolopov’s group found that the number of astrocytes increases as the number of hippocampal neural stem cells decreases, but the total sum of these two cell populations remains the same over time.