Publications by authors named "Quan Meng"

Background: Plant A/T-rich protein and zinc-binding protein (PLATZ) transcription factors are pivotal regulators in various aspects of plant biology, including growth, development, and responses to environmental stresses. While PLATZ genes have been extensively studied and functionally characterized in various plants, limited information is available for these genes in barley.

Results: Here, we discovered a total of 11 PLATZ genes distributed across seven chromosomes in barley.

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Aluminum toxicity is a major abiotic stress on acidic soils, leading to restricted root growth and reduced plant yield. Long non-coding RNAs are crucial signaling molecules regulating the expression of downstream genes, particularly under abiotic stress conditions. However, the extent to which lncRNAs participate in the response to aluminum (Al) stress in barley remains largely unknown.

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Computational super-resolution methods, including conventional analytical algorithms and deep learning models, have substantially improved optical microscopy. Among them, supervised deep neural networks have demonstrated outstanding performance, however, demanding abundant high-quality training data, which are laborious and even impractical to acquire due to the high dynamics of living cells. Here, we develop zero-shot deconvolution networks (ZS-DeconvNet) that instantly enhance the resolution of microscope images by more than 1.

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Background: Understanding gene transcription and mRNA-protein (mRNP) dynamics in single cells in a multicellular organism has been challenging. The catalytically dead CRISPR-Cas13 (dCas13) system has been used to visualize RNAs in live cells without genetic manipulation. We optimize this system to track developmentally expressed mRNAs in zebrafish embryos and to understand features of endogenous transcription kinetics and mRNP export.

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Introduction: Protein kinases play an important role in plants in response to environmental changes through signal transduction. As a large family of protein kinases, sucrose non-fermenting-1 (SNF1)-related kinases (SnRKs) were found and functionally verified in many plants. Nevertheless, little is known about the family of .

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The mechanism that initiates autophagosome formation on the ER in multicellular organisms is elusive. Here, we showed that autophagy stimuli trigger Ca transients on the outer surface of the ER membrane, whose amplitude, frequency, and duration are controlled by the metazoan-specific ER transmembrane autophagy protein EPG-4/EI24. Persistent Ca transients/oscillations on the cytosolic ER surface in EI24-depleted cells cause accumulation of FIP200 autophagosome initiation complexes on the ER.

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This study sets out to identify dysregulated plexins and investigate their roles in KIRC through an integrated bioinformatics approach. RNA-sequencing data and clinicopathological information of KIRC, extracted from The Cancer Genome Atlas (TCGA) database, were used to perform comprehensive bioinformatics analysis. Almost all plexin gene family members were dysregulated in KIRC.

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Aim: The study was designed to mine the expression and roles of IQGAP3 in clear cell renal cell carcinoma (ccRCC).

Methods: Expression profiles and clinical information were obtained from the Cancer Genome Atlas (TCGA) to estimate IQGAP3 expression in ccRCC, its relationship with patients' clinicopathological variables and prognosis, and the potential biological mechanisms.

Results: IQGAP3 was highly expressed in ccRCC and indicated advanced clinical outcome and poor prognosis.

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Aim: The aim of this study was to investigate the expression of CARS (cysteinyl-tRNA synthetase) in clear cell renal cell carcinoma (ccRCC) and its biological action mechanisms.

Methods: Expression profiles and clinical information were obtained from The Cancer Genome Atlas (TCGA) to estimate the CARS expression patterns in ccRCC, its relationship with clinicopathological variables, and prognosis of ccRCC and potential biological mechanisms in ccRCC.

Results: CARS was significantly elevated in ccRCC.

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