Stress-dependent inhibition of polarized cell growth through unbalancing the GEF/GAP regulation of Cdc42

The Arp2/3 complex promotes periodic removal of Pak1-mediated negative feedback to facilitate anticorrelated Cdc42 oscillations

“…1B). As has been reported before, we find that Cdc42 oscillations were disrupted in Lat-A treated cells, resulting in loss of CRIB-3xGFP signal at the cell ends and increased depolarized signal along the cell sides [54,55]. Lat-A treated cells displayed enhanced correlation of CRIB-3xGFP signal between cells ends (Fig.…”

Rgf1 GEF activity toward Rho1 defines a new actin-dependent signal to determine growth sites independently of microtubules and Tea1

“…To find out whether other proteins of the growth machinery also define the growth sites or if it is a specific characteristic of Rgf1, we used a mutant lacking gef1 . Gef1 is a GEF of Cdc42 involved in polarized growth and undergoes a similar relocation from poles to lateral patches under stress, where it is required to activate Cdc42 (48,49). Interestingly, the gef1 Δ tea1 Δ double mutant displayed a similar percentage of T-shaped cells as the tea1 Δ mutant, indicating that in the absence of Tea1, Gef1 is not necessary for marking the poles, in contrast to Rgf1–Rho1 (Fig 5G and S5F).…”

“…Therefore, Rgf1-Rho1 would act as Tea markers, defining growth sites without directly promoting growth, given that the tea1Δrgf1Δ double mutant retains the ability to grow, albeit at the wrong places. Interestingly, in the absence of Tea1 and Gef1 (Cdc42 GEF), which is also involved in polarized growth and relies on actin for proper localization (48)(49)(50), cells do not form branches, suggesting that is the activation of Rho1 and not that of Cdc42 which specifically defines the growth sites.…”

A stress-blinded Atf1 can fully assemble heterochromatin in a RNAi-independent minimal mat locus but impairs directionality of mat2/3 switching

“…In fission yeast, heterochromatin assembly is a requisite for proper switching of the genetic information contained at mat1 using as templates the donors mat2 or mat3 in h 90 populations, so that this switch is biased and the number of P and M cells remains almost equal, and mating and meiosis can be efficient upon nutritional deprivation. Heterochromatin assembly at mat locus is synergistically ruled by two independent pathways, and at least one of them can be modulated by environmental signals and even during a physiological cell cycle: cells lacking the Sty1 kinase display strong phenotypic defects during stress imposition, but they also have an elongated phenotype such as other cell cycle division mutants (Salat- Canela et al, 2021). We propose that the regulation of Atf1 activity by the MAP kinase cascade may be required to establish a dynamic chromatin structure favorable to both silencing but also suitable to allow the switching process at the mating-type region during an unperturbed cell cycle.…”