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Lethality was also observed for the N-terminal truncation and W557S with the muscle-specific drivers Mef2 and how24B, suggesting that the lethality associated with ubiquitous expression was likely due to expression in muscle.

This lethality was also enhanced by heat shock, thus precluding the analysis of the role of p53 in the lethality caused by Mnn1 mis-expression and stress (our unpublished results).

Moreover, lethality was also similar at low challenge dose (60% for wild type KIM D27 and 40% for the single copy dapAX complemented strain) suggesting single copy expression of dapAX is sufficient to restore virulence to near wild type levels (Figure 5A).

The biomass composition, which is very important for flux balance analysis and predicting lethality, was also recalculated and improved.

Lethality was also not correlated with drug susceptibility of Y. pestis isolates, since they were all sensitive to streptomycin, the drug recommended by the national program.

Embryonic lethality was also confirmed in the Fkbpl−/− mice because of the inability to obtain Fkbpl−/− mice with several (>50) intercrosses of Fkbpl+/− mice.

Moreover, synthetic lethality is also observed with Kar3Δ deletion.

Other non-hematopoietic defects, i.e., delay in the onset of pupariation and adult lethality, are also rescued.

Severe truncation of peripheral nerve axons and CNS axon tracts in NMNAT2-deficient embryos, likely responsible for their perinatal lethality, is also consistent with a critical axon survival function for NMNAT2 in vivo (Gilley et al., 2013; Hicks et al., 2012).

Semi-lethality was also observed for embryos containing one copy of the Gene-Switch driver strain Actin-GS-255B (data not shown).

The lethality phenotype was also observed with other M6 alleles (data not shown) and ubiquitous expression of M6-RNAi (Fig. S6 and Table S2), thus revealing an essential contribution of M6 during Drosophila development.