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Transcriptional plasticity buffers genetic variation in zinc homeostasis.

ABSTRACT: In roots of Arabidopsis thaliana, Zn can be either loaded into the xylem for translocation to the shoot or stored in vacuoles. Vacuolar storage is achieved through the action of the Zn/Cd transporter HMA3 (Heavy Metal Atpase 3). The Col-0 accession has an HMA3 loss-of-function allele resulting in high shoot Cd, when compared to accession CSHL-5 which has a functional allele and low shoot Cd. Interestingly, both Col-0 and CSHL-5 have similar shoot Zn concentrations. We hypothesize that plants sense changes in cytosolic Zn that are due to variation in HMA3 function, and respond by altering expression of genes related to Zn uptake, transport and compartmentalisation, in order to maintain Zn homeostasis. The expression level of genes known to be involved in Zn homeostasis were quantified in both wild-type Col-0 and Col-0::HMA3^CSHL-5 plants transformed with the functional CSHL-5 allele of HMA3. We observed significant positive correlations between expression of HMA3 and of genes known to be involved in Zn homeostasis, including ZIP3, ZIP4, MTP1, and bZIP19. The results support our hypothesis that alteration in the level of function of HMA3 is counterbalanced by the fine regulation of the Zn homeostasis gene network in roots of A. thaliana.

SUBMITTER: Pita-Barbosa A

PROVIDER: S-EPMC6925235 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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Transcriptional plasticity buffers genetic variation in zinc homeostasis.

Pita-Barbosa Alice A Ricachenevsky Felipe K FK Wilson Michael M Dottorini Tania T Salt David E DE

Scientific reports 20191220 1

In roots of Arabidopsis thaliana, Zn can be either loaded into the xylem for translocation to the shoot or stored in vacuoles. Vacuolar storage is achieved through the action of the Zn/Cd transporter HMA3 (Heavy Metal Atpase 3). The Col-0 accession has an HMA3 loss-of-function allele resulting in high shoot Cd, when compared to accession CSHL-5 which has a functional allele and low shoot Cd. Interestingly, both Col-0 and CSHL-5 have similar shoot Zn concentrations. We hypothesize that plants sen ...[more]

PMID: 31862901

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Project description:BackgroundThe zinc homeostasis system in Escherichia coli is one of the most intensively studied prokaryotic zinc homeostasis systems. Its underlying regulatory machine consists of repression on zinc influx through ZnuABC by Zur (Zn2+ uptake regulator) and activation on zinc efflux via ZntA by ZntR (a zinc-responsive regulator). Although these transcriptional regulations seem to be well characterized, and there is an abundance of detailed in vitro experimental data available, as yet there is no mathematical model to help interpret these data. To our knowledge, the work described here is the first attempt to use a mathematical model to simulate these regulatory relations and to help explain the in vitro experimental data.ResultsWe develop a unified mathematical model consisting of 14 reactions to simulate the in vitro transcriptional response of the zinc homeostasis system in E. coli. Firstly, we simulate the in vitro Zur-DNA interaction by using two of these reactions, which are expressed as 4 ordinary differential equations (ODEs). By imposing the conservation restraints and solving the relevant steady state equations, we find that the simulated sigmoidal curve matches the corresponding experimental data. Secondly, by numerically solving the ODEs for simulating the Zur and ZntR run-off transcription experiments, and depicting the simulated concentrations of zntA and znuC transcripts as a function of free zinc concentration, we find that the simulated curves fit the corresponding in vitro experimental data. Moreover, we also perform simulations, after taking into consideration the competitive effects of ZntR with the zinc buffer, and depict the simulated concentration of zntA transcripts as a function of the total ZntR concentration, both in the presence and absence of Zn(II). The obtained simulation results are in general agreement with the corresponding experimental data.ConclusionSimulation results show that our model can quantitatively reproduce the results of several of the in vitro experiments conducted by Outten CE and her colleagues. Our model provides a detailed insight into the dynamics of the regulatory system and also provides a general framework for simulating in vitro metal-binding and transcription experiments and interpreting the relevant experimental data.

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Transcriptional plasticity buffers genetic variation in zinc homeostasis.

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Transcriptional plasticity buffers genetic variation in zinc homeostasis.

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