our paper on what makes a biological network modular is out in Cell Systems

Here is the link (click here). Synopsis: Biological networks are highly complex, with many interconnected parts. Yet, network analysis based on small modules has proven highly effective in understanding physiological function. Our paper aims to address, at least in part, why this is the case. We show, through an analysis of the network comprising the cell cycle and pheromone pathways, that bistable switches are part of the answer. In this case, if the cell cycle switch is off, then the pheromone pathways measures the extracellular concentration unperturbed, even when the cell cycle pathway is pushed up to the bifurcation point. However, everything changes when the switch is flipped, as the cell cycle dismantles the pheromone pathway. Thus, the pheromone sensing module is unperturbed by the cell cycle in early G1 and so can be accurately modeled without including the cell cycle phase variable. Anyway, check it out. I think this subject of why motif analysis works is worth exploring since it is really not a priori obvious that it should once you think about how interconnected cellular networks are.

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