Sentence examples for mutant males expressing from inspiring English sources

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Mutant males expressing tetanus toxin (TNT) under the control of Gr68a-GAL4 hadefectfect in finding active females and a delay in courtship initiation in a large arena, but not in a small arena.

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Of note, Morsci et al. (2011) recently showed that male sexual drive in C. elegans depends on hermaphrodite self-reproductive status, because sensitized mutant males expressed more vigorous mating attempts with fog-2 mutant compared to wild-type hermaphrodites.

In brief, feminized fog-2 (q71) mutant worms lacking sperm were mated with males expressing a given centriolar protein fused to GFP, and the resulting embryos were analyzed using immunofluorescence with antibodies against GFP and the pan-centriolar marker IFA.

Notably, the eye colors of all transgenic mw+ males were lighter than that of CS males and the males expressing mw+ in the CS (w+) background displayed enhanced ethanol-induced intermale courtship levels similar to those in the w mutant background (data not shown).

Similarly, mutant males co-expressing DtorsinΔE and wild type Dtorsin transgenes exhibited a locomotion deficit that was not significantly different from that of the dtorsin KO13 larvae (UAS- dtorsin(A11) and UAS- dtorsinΔE(#12); 32.4±4.2, n = 7, not significant) (Fig. 5, column 11); UAS -dtorsin(B5) and UAS- dtorsinΔE(#21): 29.9±3.6, n = 14, not significant) (Fig. 5, column 12).

We found that dsx mutant males had significantly fewer FruM-expressing neurons in the Msg than did wild-type and control males, demonstrating that Dsx is indeed required to obtain a full complement of FruM-expressing neurons.

Mutant male larvae (dtorsin KO13) expressing wild type Dtorsin showed much improved larval locomotion.

Gal4-directed expression of DsxF in an otherwise wild-type male (also expressing DsxM) has been reported to reduce cVA levels, whereas DsxF expression in dsx mutant males abolished cVA production completely (Waterbury et al., 1999).

These considerations notwithstanding, the transgenes expressing mutant MLE proteins clearly failed to rescue mle1 mutant males.

As expected, we saw fewer cells expressing acr-5::GFP in the ventral cord of lin-39 mutant males.

To further corroborate that the unassigned ventral cord motor neurons expressing acr-5 in the wild-type males could be CA neurons, we analyzed the expression of acr-5::GFP in lin-39 mutant males.

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