The fatty acid profiles of several mutants grown at high temperature suggests that the control of flux of fatty acids from the eukaryotic pathway is partly responsible for the changes observed in 18 2 and 18 3 due to temperature.
Among several mutants unable to grow at 37°C, we explored one bearing an interruption in the URA4 gene.
Several mutants defective in silencing at core centromere, such as mis6, mis12, cnp1, mal2 and sim4, have also been shown to be defective in maintenance of the specific central core chromatin structure [38], [39], [47] [49].
Expression of several mutant proteins at 18°C resulted in an increase in their catalytic activity as well as in the amount of tetramers/oligomers; we therefore proposed that these variant proteins may be considered true folding mutations.
In the 1960s the research groups of Mertz and Nelson at Purdue University identified several mutants with increased lysine content, opaque2 (o2) and floury2 in particular, had substantially higher essential amino acid content [ 3, 4].
However, PEX5 levels were clearly reduced following growth in the dark at high temperature in several mutants (Fig. 1b), especially in pex7-2 and in the receptor-recycling mutants (pex4-1, pex2-1, and pex10-2).
Early last century, several mutants which initially seemed to have different phenotypes were recovered by the Morgan lab at Columbia University.
Several mutants also showed large and complex deletions in multiple locations within the LacI target.
We selected several mutants, each with a single gene knockout.
However, several mutants showed reduced light production.
