Research over the past decades has made immense progress in identifying some genes and mechanisms underlying plant defense against biotic organisms. The recent movement towards systems biology approaches has increased mechanistic knowledge, revealing a need for understanding how all the genes and mechanisms integrate to create a response to any given biotic interaction. This begins with evidence that diverse molecular patterns converge, suggesting that the plant perceives signals not the interacting species. These signals then coordinate across regulatory networks via molecular interactions and cause non-cell autonomous responses in neighboring and systemic cells. Finally, the identification of transporters is showing that plant defenses are harmonized across tissues and even show the potential for coordination across individuals within a population.

Bacteria in a long-term evolution experiment evolved a new metabolic trait via two separate mutations with opposite effects.

Systems studies of signal transduction pathways that modulate plant growth and immunity are rapidly identifying a large number of interactions within these pathways. These interactions are frequently presented as mechanisms allowing a plant to make proper decisions with regards to how to partition energy and resources in a proposed growth versus immunity tradeoff. This is a reinterpretation of the classical costs of resistance theory that has a long history in the ecology research community. While the ecology community is reinterpreting this theory, the reinterpretation has not been introduced into the molecular systems biology community that is studying the intersection of regulatory pathways. In this article, I describe evidence against a simple growth versus immunity tradeoff concept and propose an alternative wherein the intersection of these regulatory pathways is instead designed to coordinate these pathways, and not simply link them in mutual antagonism, to optimize fitness in complex environments where resistance/immunity and growth do not have simple linear relationships with fitness.

Transcriptomics is a major platform to study organismal biology. The advent of new parallel sequencing technologies has opened up a new avenue of transcriptomics with ever deeper and deeper sequencing to identify and quantify each and every transcript in a sample. However, this may not be the best usage of the parallel sequencing technology for all transcriptomics experiments. I utilized the Shannon Entropy approach to estimate the information contained within a transcriptomics experiment and tested the ability of shallow RNAseq to capture the majority of this information. This analysis showed that it was possible to capture nearly all of the network or genomic information present in a variety of transcriptomics experiments using a subset of the most abundant 5000 transcripts or less within any given sample. Thus, it appears that it should be possible and affordable to conduct large scale factorial analysis with a high degree of replication using parallel sequencing technologies.

Models of myriad forms are rapidly becoming central to biology. These range from statistical models that are fundamental to the interpretation of experimental results to ordinary differential equation models that attempt to describe the results in a mechanistic format. Models will be more and more essential to biologists but this growing importance requires all model users to become more sophisticated about what is in a model and how that limits the usability of the model. This review attempts to relay the potential pitfalls that can lie within a model.

A goal of metabolic engineering is to take a plant and introduce new or modify existing pathways in a directed and predictable fashion. However, existing data does not provide the necessary level of information to allow for predictive models to be generated. One avenue to reverse engineer the necessary information is to study the genetic control of natural variation in plant primary and secondary metabolism. These studies are showing that any engineering model will have to incorporate information about 1000s of genes in both the nuclear and organellar genome to optimize the function of the introduced pathway. Further, these genes may interact in an unpredictable fashion complicating any engineering approach as it moves from the one or two gene manipulation to higher order stacking efforts. Finally, metabolic engineering may be influenced by a previously unrecognized potential for a plant to measure the metabolites within it. In combination, these observations from natural variation provide a beginning to help improve current efforts at metabolic engineering.

Background

Most eukaryotic genomes have undergone whole genome duplications during their evolutionary history. Recent studies have shown that the function of these duplicated genes can diverge from the ancestral gene via neo- or sub-functionalization within single genotypes. An additional possibility is that gene duplicates may also undergo partitioning of function among different genotypes of a species leading to genetic differentiation. Finally, the ability of gene duplicates to diverge may be limited by their biological function.

Methodology/principal findings

To test these hypotheses, I estimated the impact of gene duplication and metabolic function upon intraspecific gene expression variation of segmental and tandem duplicated genes within Arabidopsis thaliana. In all instances, the younger tandem duplicated genes showed higher intraspecific gene expression variation than the average Arabidopsis gene. Surprisingly, the older segmental duplicates also showed evidence of elevated intraspecific gene expression variation albeit typically lower than for the tandem duplicates. The specific biological function of the gene as defined by metabolic pathway also modulated the level of intraspecific gene expression variation. The major energy metabolism and biosynthetic pathways showed decreased variation, suggesting that they are constrained in their ability to accumulate gene expression variation. In contrast, a major herbivory defense pathway showed significantly elevated intraspecific variation suggesting that it may be under pressure to maintain and/or generate diversity in response to fluctuating insect herbivory pressures.

Conclusion

These data show that intraspecific variation in gene expression is facilitated by an interaction of gene duplication and biological activity. Further, this plays a role in controlling diversity of plant metabolism.

Regulation of primary metabolism is a central mechanism by which plants coordinate their various responses to biotic and abiotic challenge. To identify genes responsible for natural variation in primary metabolism, we focused on cloning a locus from Arabidopsis thaliana that influences the level of TCA cycle metabolites in planta. We found that the Met.V.67 locus was controlled by natural variation in METABOLIC NETWORK MODULATOR 1 (MNM1), which encoded an AT-hook motif-containing protein that was unique to the Brassicales lineage. MNM1 had wide ranging effects on plant metabolism and displayed a tissue expression pattern that was suggestive of a function in sink tissues. Natural variation within MNM1 had differential effects during a diurnal time course, and this temporal dependency was supported by analysis of T-DNA insertion and over-expression lines for MNM1. Thus, the cloning of a natural variation locus specifically associated with primary metabolism allowed us to identify MNM1 as a lineage-specific modulator of primary metabolism, suggesting that the regulation of primary metabolism can change during evolution.