Previously, the mechanisms responsible for the longevity of IIS mutants were thought to be different from those underlying the longevity of TOR mutants or animals subjected to DR. Mutation of let- 363 (the worm TOR orthologue) together with daf- 2 does not have an additive effect on lifespan (Vellai et al. 2003) suggesting that the two pathways act by common mechanisms.
Most nonsense (insertion/deletion) mutants are thought to result in unstable transcripts and in little or no mutant protein production [ 6].
This indicates that Mad mutants previously thought to be nulls retain BMP-independent functions.
The supernumerary incisors in Wise mutants are thought to form as a result of the successive development of the rudimentary tooth germs, since apoptosis is reduced in the incisor region [41].
These high TK activity mutants are thought to simulate the conformational changes caused by activation segment phosphorylation, resulting in protein ligand-independent constitutive activation.
Moreover, certain p53 mutants are thought to acquire new functional properties that can influence gene expression levels in a manner that is unaffected by wild type p53.
SHH pathway mutations are directly associated with midline defects whereas TGF β pathway mutants are thought to act upstream of SHH, affecting SHH expression and/or activity in the prechordal plate (Rohr et al., 2001).
Interestingly, both mpk-1 mutant worms and germline deficient glp-1 mutants exhibit elevated baseline stress resistance when compared with wild type control animals., The stress resistance of glp-1 mutants is thought to reflect the general stress resistance that can be caused by a complete ablation of the reproductive germline.
The appearance of ALM posterior neurites, seen in ptrn-1 mutants, is thought to be a neuron polarity defect (Hilliard and Bargmann, 2006; Kirszenblat et al., 2013; Prasad and Clark, 2006), and the cell body puncta seen in animals expressing PTRN-1 mcherry PTRN-1 mcherrybule organizing centers necessary for polarized neurite outgrowth.
Because the NMD pathway is an mRNA surveillance mechanism, seed-size alteration in the lba1 mutant is thought to be due to altered posttranscriptional regulation of NMD-targeted gene(s) [82].
