the last banquet at the last CSHL cell cycle meeting was epic

From left to right, Rob Fisher, Stacey Blaine, Mardo Koivomagi, Jim Watson, Elizabeth Lewis, Kim Nasmyth, unknown, Amy Ikui, Clayton Schwarz, Bruce Futcher, Jon Turner

It was fun, and, I think, the first time there was an entire session on the subject of how cell growth, or cell size, acts to trigger division. The focus of several groups is now on the question of how cell size impacts the synthesis of different proteins differentially so that increased size leads to a change in the ratio of cell cycle activators to cell cycle inhibitors. Progress is happening now! Now, we just need to new meeting to talk about this at...

our paper on how the cyclin dependent kinase directly regulates cell metabolism is out in Molecular Cell

Jenny's paper is out!

Jenny shows how the major cell cycle kinase Cdk1 directly activates Nth1 to reroute carbon fluxes to promote completion of the cell cycle. Nth1 is important for utilizing carbon stored in the storage carbohydrate pool. Mobilizing this extra pool of building block can be essential when yeast are growing in poor environments. We were initially motivated to do this work from Bruce Futcher's beautiful essay on the finishing kick to Start. It turns out there is a finishing kick, but it isn't to the start of the cell cycle, but rather to push on through to the end. More broadly, this work shows how the oscillation of Cdk1 activity can directly entrain fluxes in central carbon metabolism to meet the temporally specific biosynthetic demands of the cell cycle. A similar conclusion was also reached by Bruce Futcher's group so see there paper out in the same Mol Cell issue as well. Here is a link to our paper

http://www.sciencedirect.com/science/article/pii/S1097276516001283

our paper on cell cycle evolution with the Buchler lab is out in eLife!

How can evolution change something as essential as the cell division cycle that is responsible for controlling the division of one cell into two? This is simple a function that cells can't just not have for a while. But, clearly things changed, and they changed especially drastically in the transition to the fungal lineage where the G1/S control system is dominated by components not found in animals, plants or protists. Edgar Medina and Nick Buchler found that the transition to fungi was particularly interesting, as the basal fungi retained the animal components, Rb and E2F, but also maintain the newer fungal system of Whi5 and SBF. This is the first evidence for a hybrid intermediate network, in which both systems could provide for some redundant functions and thereby facilitate more drastic evolution in this essential network. But, then, where did the newer fungal components come from? We guess viruses. For more speculation, and all the data, read the paper in eLife!

https://elifesciences.org/content/5/e09492

cell size to kinetochore ratio sets the activation of the spindle assembly checkpoint during development (Galli and Morgan Dev Cell)

A very nice paper just came out in Developmental Cell by Galli and Morgan. The show that the activation of the spindle assembly checkpoint during work development is controlled by the kinetochore-to-cell size ration. Basically, during early development, cells divide without growth to increase the ratio. There are some very nice manipulations in this paper that really help to solidify a long-standing hypothesis (that i've been aware about in the frog literature) about how the spindle checkpoint is activated during development.