Genetic interactions in yeast: is robustness going bust?

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Abstract
Mol Syst Biol. 3: 97 One of the main and naturally appealing tasks of systems biology is system's dissection and identification: knowing who does what to whom and when. A classical way to go about it in cell biology has been to knock out (delete) the genes of the system studied one by one and trace the effect that each such knockout has on the phenotype (the system's manifested behavior). In yeast (and in several other organisms), this procedure has led to the striking discovery that most of the genes are dispensable as they have negligible effects on the organism's growth rate and, hence, are apparently non‐essential. Several mechanisms have been proposed to be responsible for this observed robustness, including the existence of duplicate genes providing backups to each other, alternative metabolic and signaling pathways and an intrinsic flexibility that stems from the need to accommodate a variety of potential growth environments (Papp et al , 2004). The question of whether cellular robustness has been directly selected for as a way to avoid deleterious mutations (genetic robustness) or has evolved as a side effect of other adaptive processes such as the need to grow in different conditions (environmental robustness) has also received considerable attention (de Visser et al , 2003). In a recent paper published in Molecular Systems Biology , Jan Ihmels, Jonathan Weissman and colleagues provide an in‐depth study of one important facet of cellular robustness, focusing on the potential role of gene duplicates (paralogs) in providing backup compensation to each other (Ihmels et al , 2007 …