Sentence examples for mutants we reasoned from inspiring English sources
Given that UEV-1 does not appear to be downstream of clathrin-dependent endocytosis, and that GLR-1 colocalizes with RAB-10 in uev-1 mutants, we reasoned that UEV-1 might function in the same pathway as RAB-10.
Based on the subtle phenotypes and overall viability and fertility of uev-1 mutants, we reasoned that UEV-1 might have a smaller, more selective set of targets for K63-linked ubiquitination than would UBC-13, and that other proteins might function with UBC-13 to conduct most K63-linked ubiquitination events in nematodes.
Such mutants, we reasoned, might assist in unmasking potential functional interactions between NCS-1, CN and NFAT.
To identify potential nuclease(s) active in cdc13-1 mutants, we reasoned that genes responsible for such activities would interact with similar genes to those that EXO1 interacts with.
Due to the low penetrance of the phenotype in mir-83 (n4638 ); mir-34 (gk437 ) double mutants, we reasoned that the functions of these miRNAs in DTC migration could be relatively unimportant under standard laboratory conditions, but perhaps more critical under stressful conditions.
As rpm-1 mutant interneurons lack the presynaptic defects observed in rpm-1 mutant motorneurons, we reasoned that the postsynaptic GLR-1 trafficking defects in the rpm-1 mutant neurons might instead be due to a cell-autonomous requirement for RPM-1 activity.
Given the changes in presynaptic boutons observed in rpm-1 mutant motorneurons, we reasoned that the changes in GLR-1 ventral cord accumulation in rpm-1 mutants could reflect general defects in synapse formation on interneurons.
Since we did observe notably fewer FoxP2-labeled early born neurons in the mutant cortex, we reasoned that loss of Tsc2 in radial glia might affect their differentiation into post-mitotic neurons versus subventricular basal progenitor cells.
In order to explain the reduced osteoblast activity and the high bone resorption despite an unchanged number of cells in mutant mice, we reasoned that chondroitin sulfate proteoglycan undersulfation in the bone of dtd mice could lead to altered bone matrix quality, making the bone extracellular matrix more easily degradable by osteoclasts and slowing down matrix synthesis by osteoblasts.
As female-sterile mutants replaced female-fertile strains, we reasoned that the mutants must have a fitness advantage.
Given the enrichment of mitochondrial mutants in our Low ATP group, we reasoned that respiration deficient mutants would also be enriched in this group.
