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Unlike capn3a-knockdown embryos, which have small livers, and nid1a-knockdown embryos, which have short body lengths2, capn3a-null and nid1a-null mutants appear normal.
Similar to clp1Δ cells, lsk1Δ mutants appear normal under typical growth conditions, but display striking cytokinesis defects upon perturbation of the actomyosin ring.
Even though S310 is crucial for overall BicD phosphorylation levels, this seems not to affect BicD activity much, as Ser310 mutants appear normal, further arguing against critical roles of BicD phosphorylation on its activity.
Similar to clp1Δ cells, lsk1Δ mutants appear normal under typical growth conditions, but display severe cytokinesis defects upon perturbation of the cell division machinery.
In Hmx2, Hmx3 and Hmx2/3 null mice mutants cochlea gross structure appears unaffected, hearing capabilities in Hmx3 mutants appear normal but have not been directly tested in double mutants [ 24, 55].
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By contrast, the eyes of drep-2 mutants appeared normal.
By contrast, vulval development in ksr-1(n2526) single mutants appears normal.
While the growth of the ΔpdeH mutant appeared normal on CM agar plates (Table 2), the ΔpdeH mutant did undergo progressive autolysis of mycelia after prolonged incubation for at least 14 days (Figure 2, top panel).
In contrast, type I neuroblast clones of this double mutant appeared normal, as there was only one neuroblast per clone.
By the age of 1 year, Muc16 homozygous mutant mice appear normal.
Intriguingly, all the defects we observe are limited to clone boundaries; cells fully within the mutant clones appear normal.
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