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Also, known arrhythmic biological mutants of the circadian clocks seem to result from a severe structural change in the underlying network, rather than from normal mode of operation under certain environmental conditions [33].
The simulations of the mutants were compared to experimental phenotypes of the corresponding biological mutants.
We are currently trying to test this hypothesis by using combination of biological mutants such as the Δ gsh1.
Indeed, several is-mutant do not accumulate ROS, while the corresponding biological mutants were reported as sensitive to oxidative stress.
These large deletions may be real biological mutants or they could be amplification or sequencing artifacts (e.g. chimeras).
The "phenotypes" of such mutants were found to be consistent with published data for the phenotypes of the corresponding biological mutants, providing the first demonstration that our model was of high quality.
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The biological mutant exhibits apparently contradictory phenotypes, with increased ethanol accumulation and increased respiratory growth.
Our model did not allow to evidence accumulation of zinc in a is-zrt1 mutant, but this phenotype reported in SGD was conditional to the presence of aluminum ions in the growth medium of the biological mutant [ 44].
We show the evolution of the PoP during the simulations for selected elements in representative mutants in Figure 4. Figure 4-A describes a simple situation in which deletion of the gene encoding ferrochelatase (is-hem15) leads to an increase in the PoP of protoporphyrin IX, the substrate of the enzyme, paralleling the situation occurring in vivo in the corresponding biological mutant [ 40].
Figure 7-D shows that under this hypothesis, most of the phenotypes of the biological yfh1 mutant are appropriatly described in the model since in this mutant, the glutathione PoP is 0% at steady state: there is a strong increase of the PoP of FePi in addition to the previously observed high PoP of ROS, loss of iron-sulphur clusters and drop in mitochondrial glutathione.
We describe a set of rules for naming chromosomes and identifying loci, genes, and alleles based on biological function, mutant phenotype, and sequence identity, and suggest ways of dealing with aliases (synonyms), sequence variants, and loci identified by multiple annotations of the genome assemblies available from various sources.
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Since I tried Ludwig back in 2017, I have been constantly using it in both editing and translation. Ever since, I suggest it to my translators at ProSciEditing.

Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com