We selected mutants spread over the entire protein: some of the mutations are located at the subunit-subunit interface, some add a positively charged residue, others substitute an hydrophobic residue with an hydrophilic one, or some produce a simple side chain size variation.
In any case the new, more efficient mutant spreads, and the metabolic system itself also benefits.
Cells expressing the S188/190A mutant spread slower than those expressing wild-type paxillin (Fig. 3B).
Interestingly, although the majority of esco2 mutant spreads had complete chromatid separation, 15% of spreads yielded a PBS morphology.
In the present study, we observe that cells expressing EGFP-S188/190A paxillin mutant spread less but migrate more on collagen than control cells.
Under the "costly female trait" hypothesis the mutant spreads because females homozygous for the mutation are assumed to be fitter than non mutant females, while no cost assumptions are required under the "functional virginity mutation" hypothesis.
In an effort to understand the physiological relevance of paxillin protection from degradation, we show that cells expressing the paxillin S188/190A interfering mutant spread less, have reduced protrusive activity but migrate more actively.
Cheater strains in the Dictyostelidae typically have a fitness cost or some deleterious pleiotropic effect that prevents the mutant from spreading, since otherwise a loss of function mutant would easily evolve.
With or without high relatedness, disadvantageous pleiotropic effects can also keep a mutant from spreading [ 27].
