Fig. 5

Comparison of data from CR, CAS, ZYM and published cell integrity related phenotypic screenings. The complete gene set of 636 genes identified in our screenings was compared to data from the following published large-scale phenotypic screenings: sensitivity against K1 and K2 killer toxins which bind to different cell wall receptors, ultimately forming lethal pores in the plasma membrane [27, 86]; chitosan, a deacetylated derivative of chitin which eventually causes plasma membrane stress accompanied by structural changes in the cell wall [87]; freeze-thaw or heat stress, which have been related to defects in cell wall biogenesis or assembly [88, 89]; aluminum, the small glycopeptide antibiotic bleomycin or acidic conditions, for which a proper cell wall maintenance and architecture appears to play an important protective role [90–92]; detection of low dye binding (ldb) phenotypes associated with altered mannoprotein-linked oligosaccharides located in the outer layer of the cell wall [93]; altered budding pattern [94] and morphological phenotypes [95]. A graphical representation of this comparison is shown. Vertical axis corresponds to the different conditions analyzed, and genes whose deletion cause a phenotype of hypersensitivity (labelled in red) in at least eight of the conditions analyzed are represented in the horizontal axis. Black indicates absence of hypersensitivity phenotype