Sentence examples for mutants reflects a from inspiring English sources

DOI: http://dx.doi.org/10.7554/eLife.03467.012 The requirement for SPO-11 in tethering sister chromatids in rec-8 mutants reflects a need for DSBs, since SCC was restored in spo-11 rec-8 mutants treated with γ-irradiation.

We next investigated whether the failure to initiate pouch outpocketing in tbx1 mutants reflects a loss of segmental character in the pre-pouch endoderm, or instead defects in the morphogenesis of pre-specified segmental units.

Thus, the increased axon regrowth of efa-6 mutants reflects a complete loss of EFA-6 function, and the major activity of EFA-6 in axon growth resides in the N-terminus, dependent on the 18 aa motif.

To assess whether the low level of TCP-1α observed in mst mutants reflects a reduction of the entire TCP-1 complex, we subjected wild-type and mst mutant larval extracts to size exclusion chromatography, probing separated fractions for TCP-1α.

The numerous changes in cell wall structures found in the lrx mutants reflects a general problem in the analysis of cell wall mutants: the difficulty to distinguish between primary effects of the mutations under investigation and the secondary effects induced by the plant with the aim of compensating the primary changes.

We cannot completely exclude the possibility that changes in COL1 deposition in bat mutants reflects a non-specific reduction of ECM molecules as a consequence of FRAS1-FREM-complex disruption; however, the reduced COL1 deposition observed is consistent with the associations between COL1 and both PDGFC and TIMP1 reported in the literature (Lai et al., 2011; Yokose et al., 2012).

Given the absence of even a minimal suppression, it seems unlikely that the loss of commissures and/or AEP defects noted in our mutants reflects an increase in Robo-dependent midline repulsion.

Some of the dispersed spreads we observe in zip1Δ mutants reflect a role for Zip1 in pairing the centromeres of homologous chromosomes in late prophase [14], [19], [20], [21].

The IIS pathway mutants reflect a correlation between longevity and stress resistance.

Detailed analysis of the structure indicates that the tighter binding in the mutant reflects a shift in the conformational equilibrium of the substrate-free enzyme towards the conformation seen in the substrate complex rather than differences in the enzyme substrate interactions.

We speculate that the chromosome missegregation we observe in the vfl2 mutant reflects a decreased effectiveness of acentriolar spindles that self-assemble in this mutant.