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We tested loss of function alleles for five of these genes (all that were available), but did not observe a genetic interaction with any of them (Table S2).
We therefore tested loss of function alleles for Sc2, ida and mge (all of the Eip63F-1 areeles are viable) and found SSNC between Sc21 and Rho1E(bRho1E, Rho1E(br)233 and Rho1E3.10 (Table 2 and Table S2).
Two predictive criteria were tested: loss of body weight during feed deprivation and compensatory growth during re-feeding.
Of the promoters tested, loss of HP1a significantly reduced H3K4me3 levels at nine genes; lt was unchanged although cta, which is also in heterochromatin, did show a drop.
The tested loss from brine was based on NaCl; the viscosity change at different salinities was illustrated in the simulation.
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Of the three alleles tested, loss-of-function th4 and th5 and gain-of-function th6-3s, only th4 strongly enhanced the CUG toxicity phenotype (Figure 5F).
AGB1 plays a positive role in the UPR response [ 49], since three tested loss-of-function agb1 mutants showed hypersensitivity to tunicamycin (note that an earlier report by Wang et al. [ 55] describing the opposite agb1 UPR phenotype could not be reproduced) [ 49].
Terminal anaesthesia was confirmed by testing loss of the pedal reflex.
Alternatively, species spectra that contrast traits of endemic vs. indigenous (Vargas et al. 2014) and congeneric species pairs (Vazačová and Münzbergová 2014) have already been used to test loss of dispersability.
Given the reports of reduced GluN2C expression in the DLPFC of schizophrenia patients18,21,22 we tested whether loss of GluN2C resemble the neuropathologies observed in schizophrenia patients.
We tested whether loss of yar affected homeostasis.
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