During the course of cloning, we noticed that the initial D40 clone had a deletion of a nucleotide in the middle of the coding region that leads to an occurrence of a stop codon several bases downstream of the deletion (Takimoto, 1999).
While comparing the results of PCR sequencing and clone sequencing, we noticed an interesting phenomenon.
Among the founder clone mutations, we noticed a BRCA1 nonsense mutation, which may explain the high mutation rate observed in this sample.
When working with these various clones in our laboratory, we noticed several differences in their cellular morphology and behavior, which led us to perform a functional comparison with regard to cell growth in vitro and in vivo, clonogenicity, and radiation resistance.
When comparing the cDNA of the initially cloned mouse ADAR2R sequence, we noticed an A-to-G discrepancy changing a genomically encoded Arginine codon (AGG) to a Glycin codon (GGG).
We noticed sdAb clones B2, B3, B5, B7, B17 and B18 were capable of detecting toxin when used alone and also capable of detecting complex alone, as were B4, B6, B10, B13, B14 and B20.
We noticed that clones in the midgut sometimes run for a considerable distance perpendicular to the a/p axis, but rarely if ever parallel to the axis.
Intriguingly, we noticed that clones located in the medial region, where the neocortex bends, exhibited a higher ratio of d2/d1 than those in the dorsal and lateral regions, indicating a potential link between clone shape and local geometry of the neocortex.
In the rescreening of this line, we noticed that clones outside of the germarium typically included one or more cells within the stalk plus a small cluster of polar and/or follicle cells on the anterior of the follicle at the point of stalk attachment.
In addition, we noticed LacZ+ germ cell clones with the TIE-DYE clone system, indicating that line 688A also expresses Flp in the germline.
