In summary, we propose the following overall model to integrate our current observations with previous studies: In most cell lines, relatively low levels of HSP90 inhibitors induce G1 accumulation through destabilization of sensitive growth-factor receptors and subsequent loss of mitogenic signaling.
Even a single irrigation omission during one of the sensitive growth stages, caused up to 40% grain yield losses during dry years such as 1996.
One of the most sensitive growth metrics relies on flow cytometry to monitor growth of fluorescently tagged strains, allowing fitness differences of 1% to be reproducibly discerned (Breslow et al. 2008).
C. vulgaris was generally most sensitive; growth, especially of roots, was strongly affected in A. nodiflorum; growth rate of M. spicatum was sensitive to diuron.
By deleting regions of Ysp2p, we found that rescue of AmB-sensitive growth was affected most upon removing either the C-terminal anchor or the second StART-like domain.
Such features should cause a distribution of microstructure-sensitive growth rates.
In the present study, we isolated rho3+, which encodes a Rho-family small GTPase, an important regulator of exocystosis, as a multicopy-suppressor of the temperature-sensitive growth of the apm1-1 mutant cells.
We identified rpn3 -L140P, which encodes a component of the 19S proteasomal regulatory particle of the 26S proteasome, as a suppressor of the temperature-sensitive growth caused by mec1 -W2368A.
The complementation or multicopy suppression of the temperature-sensitive growth phenotypes was assayed by transforming plasmids expressing the wild type, mutant versions of SSO1 or SSO2 or the empty vector to sso2Δ GAL1-straintrain (H3664) or to sso mutant strains H2177 and H2608.
We also examined the effects of these plasmids on the temperature-sensitive growth of Δrho3 cells.
Given that a tolC strain does not appear to express the glutamate-dependent acid resistance system, we assessed the contribution of the Gad system to the pH-sensitive growth of a tolC mutant.
