Cell cycle regulation by stress-activated MAP kinases (SAPK) is one of the general mechanisms of response to stress that are critical for cell survival

Previous works by the lab in S. cerevisiae showed that SAPKs can act at different cell cycle phases to respond promptly to extracellular stimuli and maintain cell integrity.

In particular, Hog1 activation during G1 is responsible for stabilization of Sic1 (Escote’ et al., 2004), down-regulation of G1/S cyclin expression (Androver et al., 2011) and inhibition of G1 cyclin expression via phosphorylation of the transcription factors Whi5 and Msa1 (Gonzalez-Novo et al., 2015). Later on, work from this lab showed similar regulation of G1 in mammalian cells upon osmostress (Joaquin et al., 2012)(Figure 1A).

During S-phase, Hog1 activation causes a delay in Clb5 and Clb6 accumulation (Yaakov et al., 2009) (Figure 1A) and direct phosphorylation of Mrc1 delays Cdc45 loading preventing conflicts between DNA replication and transcription (Duch et al., 2013) (Figure 1B).

Finally, in G2 phase, SAPK activation leads to stabilization of cell cycle inhibitor Swe1 by phosphorylation of Hsl1 (Clotet et al., 2006) (Figure 1C).

Currently, the Cell Cycle Unit focuses in acquiring new insights into the stress dependent S-phase delay and exploring a potential regulatory role of SAPK during mitosis and cell division.