Sentence examples for lethality is likely from inspiring English sources

Exact(1)

Consistent with this observation, expression of UAS-Wnt6 with various GAL4 drivers such as patchedts-GAL4 (with GAL80ts) and nubbin-GAL4 cause pupal lethality; however, this does not yield obvious morphological defects in the resulting wings (not shown), suggesting that the lethality is likely due to expression in other parts of the body.

Similar(59)

This lethality was likely associated with a strikingly greater extent of lung injury including pronounced leukocyte infiltration of the interstitial and alveolar spaces, edema and alveolar distortion observed within 12 h after LPS injection (Fig  7E).

Differences between breeding schedules, which significantly influence the magnitude and sex-specificity of the effects of Tex19.1 −/− on embryonic lethality, are likely to account for differences between the data in Supplementary Material, Table S1 and previously published observations (37).

These results support the idea that gametes are unaffected by Ospie1-1 and Ospie1-2 mutandons and that the homozygous lethality of Ospie1 mutants is likely caused by a defect in embryo development.

While these studies can not rule out transient fork progression defects, at present we find no evidence that ctf7 rad61 ctripleriple mutants exhibit gross S-phase progression defects, consistent with the notion that the conditional lethality of these cells is likely a result of increased cohesion defects.

But the hint of lethality, if not altogether gone, is likely to be attenuated.

Together, these considerations suggest that the lethality of the dRecQ4 mutants is likely a consequence of loss of both of its primary functions, namely DNA replication and DNA repair.

The L1 lethality seen in the apl-1 tm385 apl-1 tm385likely due, at leastrainpart, to the moltisg defect, which is recapitulikelyby apl-1 RNAi.

The low level lethality observed for noca-1 RNAi) noca-1 RNAilikembryosecondary consequence of the effect of NOCA-1 depletisn on germlikelytructure.

Since we observed that the severity/onset of Smn-dependent mortality (Figure 3) corresponds to the degree of NMJ defects (Figure 5), we reasoned the identification of enhancers and suppressors of Smn73Ao-dependent lethality would be likely to yield genes that also function at the NMJ.

The failure of proper cell cycle progression and proliferation is likely to be the cause of lethality.

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