Gαs is expressed in the forming nervous system of Drosophila embryos, and absence or mutation of Gαs is lethal during development [34], suggesting that Gαs-dependent modulation of cAMP levels can play a critical role in a wide variety of neuronal processes throughout development.
The knockout of Dnmt1, which has a strong preference for hemimethylated DNA and is thus considered to be a maintenance DNA methyltransferase, is lethal during development [ 14].
However, because the Rptor knockout was lethal during development, we were unable to use genetics to assess this possibility in adult animals.
cIV knockdown in neurons was not lethal during development but produced a rapidly progressing locomotor and seizure-sensitivity phenotype, which was substantially alleviated by AOX.
In Drosophila, even severe neurodegenerative phenotypes associated with mitochondrial dysfunction, are non-lethal during development (48, 49).
In contrast, disruption of DOHH in D. melanogaster is lethal early in development (Patel et al., 2009), suggesting that the maturation of eIF5A(Dhp50) to eIF5A Hyp50), catalysed by DOHH activity, might be crucial for the viability of higher eukaryotes.
For T. gratilla, 30°C approximates the lethal threshold for development in both high and low latitude populations [41, this study].
This is in stark contrast to animals lacking Tsc1, Tsc2, Akt, or Rheb, all of which are lethal early in development [14] [18].
Their inhibition or knockout is lethal in early development.
Non-small cell lung cancer (NSCLC) remains lethal despite the development of numerous drug therapy technologies.
