Dataset Information

Dynamical compensation in physiological circuits.

ABSTRACT: Biological systems can maintain constant steady-state output despite variation in biochemical parameters, a property known as exact adaptation. Exact adaptation is achieved using integral feedback, an engineering strategy that ensures that the output of a system robustly tracks its desired value. However, it is unclear how physiological circuits also keep their output dynamics precise-including the amplitude and response time to a changing input. Such robustness is crucial for endocrine and neuronal homeostatic circuits because they need to provide a precise dynamic response in the face of wide variation in the physiological parameters of their target tissues; how such circuits compensate their dynamics for unavoidable natural fluctuations in parameters is unknown. Here, we present a design principle that provides the desired robustness, which we call dynamical compensation (DC). We present a class of circuits that show DC by means of a nonlinear feedback loop in which the regulated variable controls the functional mass of the controlling endocrine or neuronal tissue. This mechanism applies to the control of blood glucose by insulin and explains several experimental observations on insulin resistance. We provide evidence that this mechanism may also explain compensation and organ size control in other physiological circuits.

SUBMITTER: Karin O

PROVIDER: S-EPMC5147051 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature

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Dynamical compensation in physiological circuits.

Karin Omer O Swisa Avital A Glaser Benjamin B Dor Yuval Y Alon Uri U

Molecular systems biology 20161108 11

Biological systems can maintain constant steady-state output despite variation in biochemical parameters, a property known as exact adaptation. Exact adaptation is achieved using integral feedback, an engineering strategy that ensures that the output of a system robustly tracks its desired value. However, it is unclear how physiological circuits also keep their output dynamics precise-including the amplitude and response time to a changing input. Such robustness is crucial for endocrine and neur ...[more]

PMID: 27875241

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Project description:The formation of new species is often a consequence of genetic incompatibilities accumulated between populations during allopatric divergence. When divergent taxa interbreed, these incompatibilities impact physiology and have a direct cost resulting in reduced hybrid fitness. Recent surveys of gene regulation in interspecific hybrids have revealed anomalous expression across large proportions of the genome, with 30-70% of all genes apparently misexpressed, mostly in the direction of down-regulation. However, since most of these studies have focused on pairs of species exhibiting high degrees of reproductive isolation, the association between regulatory disruption and reduced hybrid fitness prior to species formation remains unclear. Within the copepod species Tigriopus californicus, interpopulation hybrids show reduced fitness associated with mitochondrial dysfunction. Here we show that in contrast to studies of interspecific hybrids, only 1.2% of the transcriptome was misexpressed in interpopulation hybrids of T. californicus, and nearly 80% of misexpressed genes were overexpressed rather than underexpressed. Moreover, many of the misexpressed genes were components of functional pathways impacted by mitonuclear incompatibilities in hybrid T. californicus (e.g., oxidative phosphorylation and antioxidant response). We also show that the magnitude of hybrid misregulation is not dependent on levels of protein sequence divergence, even though the latter is correlated with expression divergence between parental populations. Our results suggest that hybrid breakdown at early stages of speciation may result from initial incompatibilities amplified by the cost of compensatory physiological responses. Our experiment included nine RNA-seq samples: 3 San Diego, 2 Santa Cruz, and 4 hybrid samples. For each sample, 400-500 copepods across all developmental stages were collected from their stock cultures. They were transferred to fresh filtered seawater in a 50-mL Falcon tubes and immersed in a 20°C water bath for two hours. Water was then quickly removed, 4 mL of Tri-Reagent (Sigma) added, and tissue immediately disrupted using a tissue homogenizer. RNA was isolated following the manufacturer’s protocol. Re-suspended RNA pellets were further purified with RNeasy Mini columns (Qiagen), and final sample integrity and quantity were assessed with an Agilent 2100 BioAnalyzer. Please note that two samples (GSM1531288, GSM1531290) have been accessioned under BioProject PRJNA168170, SRA study SRP013608, while the remaining seven samples under BioProject PRJNA263967, SRA Study SRP048974. The current records including all 9 samples (PRJNA264820/SRP049247) were re-created for the convenient retrieval of the complete raw data from SRA

Dataset Information

Dynamical compensation in physiological circuits.

Publications

Dynamical compensation in physiological circuits.

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