44 research outputs found

    Gene network analysis of poplar root transcriptome in response to drought stress identifies a PtaJAZ3PtaRAP2.6-centered hierarchical network

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    Using time-series transcriptomic data from poplar roots undergoing polyethylene glycol (PEG)-induced drought stress, we built a genetic network model of the involved putative molecular responses. We found that the network resembled a hierarchical structure. The highest hierarchical level in this structure is occupied by 9 genes, which we called superhubs because they were primarily connected to 18 hub genes, which are then connected to 2,934 terminal genes. We were only able to regenerate transgenic plants overexpressing two of the superhubs, suggesting that the majority of the superhubs might interfere with the regeneration process and did not allow recovery of transgenic plants. The two superhubs encode proteins with closest homology to JAZ3 and RAP2.6 genes of Arabidopsis and were consequently named PtaJAZ3 and PtaRAP2.6. PtaJAZ3 and PtaRAP2.6 overexpressing transgenic lines showed a significant increase in both root elongation and lateral root proliferation and these responses were specific for the drought stress conditions and were highly correlated with the levels of overexpression of the transgenes. Several lines of evidence suggest of regulatory interactions between the two superhubs. Both superhubs were significantly induced by methyl jasmonate (MeJA). Because jasmonate signaling involves ubiquitin-mediated proteasome degradation, treatment with proteasome inhibitor abolished the MeJA induction for both genes. PtaRAP2.6 was upregulated in PtaJAZ3 transgenics but PtaJAZ3 expression was not affected in the PtaRAP2.6 overexpressors. The discovery of the two genes and further future insights into the associated mechanisms can lead to improved understanding and novel approaches to regulate root architecture in relation to drought stress

    Qubit-excitation-based adaptive variational quantum eigensolver

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    Abstract: Molecular simulations with the variational quantum eigensolver (VQE) are a promising application for emerging noisy intermediate-scale quantum computers. Constructing accurate molecular ansĂ€tze that are easy to optimize and implemented by shallow quantum circuits is crucial for the successful implementation of such simulations. AnsĂ€tze are, generally, constructed as series of fermionic-excitation evolutions. Instead, we demonstrate the usefulness of constructing ansĂ€tze with "qubit-excitation evolutions”, which, contrary to fermionic excitation evolutions, obey "qubit commutation relations”. We show that qubit excitation evolutions, despite the lack of some of the physical features of fermionic excitation evolutions, accurately construct ansĂ€tze, while requiring asymptotically fewer gates. Utilizing qubit excitation evolutions, we introduce the qubit-excitation-based adaptive (QEB-ADAPT)-VQE protocol. The QEB-ADAPT-VQE is a modification of the ADAPT-VQE that performs molecular simulations using a problem-tailored ansatz, grown iteratively by appending evolutions of qubit excitation operators. By performing classical numerical simulations for small molecules, we benchmark the QEB-ADAPT-VQE, and compare it against the original fermionic-ADAPT-VQE and the qubit-ADAPT-VQE. In terms of circuit efficiency and convergence speed, we demonstrate that the QEB-ADAPT-VQE outperforms the qubit-ADAPT-VQE, which to our knowledge was the previous most circuit-efficient scalable VQE protocol for molecular simulations

    Variational quantum chemistry requires gate-error probabilities below the fault-tolerance threshold

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    The variational quantum eigensolver (VQE) is a leading contender for useful quantum advantage in the NISQ era. The interplay between quantum processors and classical optimisers is believed to make the VQE noise resilient. Here, we probe this hypothesis. We use full density-matrix simulations to rank the noise resilience of leading gate-based VQE algorithms in ground-state computations on a range of molecules. We find that, in the presence of noise: (i) ADAPT-VQEs that construct ansatz circuits iteratively outperform VQEs that use "fixed" ansatz circuits; and (ii) ADAPT-VQEs perform better when circuits are constructed from gate-efficient elements rather than physically-motivated ones. Our results show that, for a wide range of molecules, even the best-performing VQE algorithms require gate-error probabilities on the order of 10−610^{-6} to 10−410^{-4} to reach chemical accuracy. This is significantly below the fault-tolerance thresholds of most error-correction protocols. Further, we estimate that the maximum allowed gate-error probability scales inversely with the number of noisy (two-qubit) gates. Our results indicate that useful chemistry calculations with current gate-based VQEs are unlikely to be successful on near-term hardware without error correction.Comment: 17 pages, 8 figure

    EARLY BUD-BREAK 1 and EARLY BUD-BREAK 3 control resumption of poplar growth after winter dormancy

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    Bud-break is an economically and environmentally important process in trees and shrubs from boreal and temperate latitudes, but its molecular mechanisms are poorly understood. Here, we show that two previously reported transcription factors, EARLY BUD BREAK 1 (EBB1) and SHORT VEGETATIVE PHASE-Like (SVL) directly interact to control bud-break. EBB1 is a positive regulator of bud-break, whereas SVL is a negative regulator of bud-break. EBB1 directly and negatively regulates SVL expression. We further report the identification and characterization of the EBB3 gene. EBB3 is a temperature-responsive, epigenetically-regulated, positive regulator of bud-break that provides a direct link to activation of the cell cycle during bud-break. EBB3 is an AP2/ERF transcription factor that positively and directly regulates CYCLIND3.1 gene. Our results reveal the architecture of a putative regulatory module that links temperature-mediated control of bud-break with activation of cell cycle. An AP2/ERF family gene EBB1 and a MADS-box gene SVL encode two regulators of poplar bud break. Here, the authors report another AP2/ERF transcription factor EBB3, which functions together with EBB1, SVL, and cell cycle progression promoter CYCD3.1 to regulate poplar bud break

    The AINTEGUMENTA LIKE1

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    Adventitious rooting is an essential but sometimes rate-limiting step in the clonal multiplication of elite tree germplasm, because the ability to form roots declines rapidly with age in mature adult plant tissues. In spite of the importance of adventitious rooting, the mechanism behind this developmental process remains poorly understood. We have described the transcriptional profiles that are associated with the developmental stages of adventitious root formation in the model tree poplar (Populus trichocarpa). Transcriptome analyses indicate a highly specific temporal induction of the AINTEGUMENTA LIKE1 (PtAIL1) transcription factor of the AP2 family during adventitious root formation. Transgenic poplar samples that overexpressed PtAIL1 were able to grow an increased number of adventitious roots, whereas RNA interference mediated the down-expression of PtAIL1 expression, which led to a delay in adventitious root formation. Microarray analysis showed that the expression of 15 genes, including the transcription factors AGAMOUS-Like6 and MYB36, was overexpressed in the stem tissues that generated root primordia in PtAIL1-overexpressing plants, whereas their expression was reduced in the RNA interference lines. These results demonstrate that PtAIL1 is a positive regulator of poplar rooting that acts early in the development of adventitious roots

    Members of the LATERAL ORGAN BOUNDARIES DOMAIN Transcription Factor Family Are Involved in the Regulation of Secondary Growth in Populus[W]

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    This work reports the isolation and characterization of a novel gene of the LBD family of transcription factors, which regulates phloem development during secondary woody growth of a poplar tree. This discovery reveals a novel regulatory step that directs secondary woody growth and is likely mediated through auxin signaling and suppression of meristem and/or activation of phloem identity genes
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