Mutations are ordered on the tree according to their relative age.
Magenta (MCF > 5%, present) and blue (absent) mutations are ordered by time information, indicating the status of the corresponding alterations.
At such mutagenesis frequencies the number of induced mutations is orders of magnitude above the accumulation of spontaneous mutations, yet is not too large as to preclude organismal viability [1].
Peptides (p63 TA1 [9-32] and p63 TA1Fwithithetripleiple mutation F16A, W20A, L23A and mutation F10W) were ordered from Genscript (Piscataway, NJ, USA).
Mast cells were positive for CD2 and CD25 expression by immunohistochemistry. Targeted genomic analysis for mutations in KIT was ordered, but ultimately failed due to insufficient sample material.
Cancer types and subgroups are ordered by increasing mutation frequency median, with the lowest frequencies (left) found in pediatric tumors and low-grade NF1-glioma.
The PTPRS expression vectors containing various site and deletion mutations were also customarily ordered from GeneCopoeia.
In the linear evolution model, we assumed that all mutations were mutated in a linear order shown in the left panel of Figure 2A.
A first group of mutations were designed in order to disrupt putative interactions between the agonist and the binding pocket (Figure S3).
The double mutant control mutations were screened in order to maintain the same notional melting temperature (Tm) as the wild-type Tm.
