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Predicting molecular responses in human by extrapolating results from model organisms requires a precise understanding of the architecture and regulation of biological mechanisms across species.
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Both model organisms require further characterization of the neurological defects caused by NPC1 protein deficiency.
The establishment of a model organism requires many resources.
Cross utilization of genomic tools to infer phylogenies in non-model organisms requires resolution of a fundamental conflict between the need to identify genomic sequences that are conserved (largely or wholly) across many divergent taxa, and the need to identify DNA-level differences that reflect the evolutionary history at the desired taxonomic level.
Gene expression studies on non-model organisms require open-end strategies for transcription profiling.
To apply the model above to non-haploid organisms requires some adjustments to account for the fact that duplicate copies of genes can buffer deleterious effects.
Development in multicellular organisms requires the organized generation of differences.
For a functional assessment, expert knowledge about a suitable test essay or genetically modified model organisms is required.
Genome sequencing projects were long confined to biomedical model organisms and required the concerted effort of large consortia.
Obtaining SNPs in model organisms has required further sequencing efforts (e.g., Wicks et al. 2001), some of which did not come about for nearly a decade after the initial genome release (Langley et al. 2012; Mackay et al. 2012; Sackton et al. 2009).
We consider a microbial population model in which organisms require two metabolites A and B in order to grow and reproduce.
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