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Moreover, mod-1 mutant animals do not show a defective response to starvation (Fig. 4).
Furthermore, we show with electron microscopy that cilia in MKS3 mutant animals do not manifest the proper microtubule architecture.
Although cat-2 mutant animals do not completely lack endogenous DA (they still synthesize ∼40% of wild-type C. elegans DA levels), this is similar to what is seen in tyrosine hydroxylase-deficient mice [35], [37].
Consistent with our model, we found that animals expressing Wnt both from endogenous loci and from the transgene show a mild but significant underextension phenotype (10% of the animals), whereas transgenic mutant animals do not (Fig. 3L).
Tsc1 mosaic pupae show severe axon guidance abnormalities and Tsc1 mutant animals do not survive to the pupal stage; in contrast, animals bearing both a Tsc1 mutation and a hypomorphic Tor allele survived to pupal stages and showed only modest axon guidance abnormalities in larval and pupal brains (Figure 6G, H, Table 1).
Although they are viable, per mutant animals do not exhibit circadian gene expression or behavioral rhythmicity.
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In contrast, the majority of acs-22 mutant animals did not have increased Hoechst permeability.
The reduced numbers of mature neurons in the hippocampus and ventral midbrain of Ngn2 null mutant animals does not appear to be due to cell death or migration defects [20], [31].
Importantly, while dop-1 mutant animals did not show a defect and responded similarly to wild-type animals, loss of DOP-1 countered loss of DOP-3; a role for DOP-1 was only revealed when examined in combination with loss of DOP-3 [25].
However, buffy mutant animals did not have more mitochondria since no increase in mitochondrial genomes was observed in larval or fat body extracts (unpublished observations, JPM and CBB).
In snt-1 unc-104 snt-1 unc-104 snt-1 unc-104GFP signal accumulatedoubleell bodies like in unc-104 single mutants, suggestheg that further removal of SNB-1 GFPnc-104 SNB-1 GFPmalsignal not accumulatedependence of SVs on UNC-104 for intracellular trafficking.
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