Reconstruction of a yeast pan-genome-scale metabolic model for evolutionary systems biology

2016 ◽  
Vol 33 ◽  
pp. S14
Author(s):  
Kevin Correia ◽  
Peter Li ◽  
Lilly Yu ◽  
Radhakrishnan Mahadevan
2021 ◽  
Vol 12 ◽  
Author(s):  
Sander Y. A. Rodenburg ◽  
Michael F. Seidl ◽  
Dick de Ridder ◽  
Francine Govers

Metabolism is the set of biochemical reactions of an organism that enables it to assimilate nutrients from its environment and to generate building blocks for growth and proliferation. It forms a complex network that is intertwined with the many molecular and cellular processes that take place within cells. Systems biology aims to capture the complexity of cells, organisms, or communities by reconstructing models based on information gathered by high-throughput analyses (omics data) and prior knowledge. One type of model is a genome-scale metabolic model (GEM) that allows studying the distributions of metabolic fluxes, i.e., the “mass-flow” through the network of biochemical reactions. GEMs are nowadays widely applied and have been reconstructed for various microbial pathogens, either in a free-living state or in interaction with their hosts, with the aim to gain insight into mechanisms of pathogenicity. In this review, we first introduce the principles of systems biology and GEMs. We then describe how metabolic modeling can contribute to unraveling microbial pathogenesis and host–pathogen interactions, with a specific focus on oomycete plant pathogens and in particular Phytophthora infestans. Subsequently, we review achievements obtained so far and identify and discuss potential pitfalls of current models. Finally, we propose a workflow for reconstructing high-quality GEMs and elaborate on the resources needed to advance a system biology approach aimed at untangling the intimate interactions between plants and pathogens.


2009 ◽  
pp. 331-349 ◽  
Author(s):  
Christina L. Richards ◽  
Yoshie Hanzawa ◽  
Manpreet S. Katari ◽  
Ian M. Ehrenreich ◽  
Kathleen E. Engelmann ◽  
...  

2017 ◽  
Author(s):  
Li Ma ◽  
Angelo Hoi Chung Chan ◽  
Jake Hattwell ◽  
Paul R. Ebert ◽  
Horst Joachim Schirra

AbstractBackgroundPest insects are increasingly resistant to phosphine gas, which is used globally to protect grain reserves. The enzyme dihydrolipoamide dehydrogenase (DLD) is a phosphine resistance factor and participates in four key steps of core metabolism, making it a potential central metabolic regulator.ResultsHere we used microarray data and NMR-based metabolomics to characterize the phosphine response of wild-type C. elegans and the phosphine-resistant strain dld-1(wr4) which has a partial loss-of-function mutation in the gene for DLD. In addition, we have constructed CeCon, a C. elegans genome-scale metabolic model to facilitate integration of gene expression and metabolomics data.ConclusionsThe resulting systems biology analysis is consistent with the hypothesis that adaptation to a hypometabolic state is the most prominent mechanism of phosphine resistance in this nematode strain. The involvement of DLD in regulating and creating hypometabolic adaptation has implications for other biological phenomena involving hypometabolism, such as reperfusion injury and metabolic resistance.


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