Biology subjects

Wang, Z.-Q.

Publications and source records attributed to Wang, Z.-Q..

5 recordsLinked to original sources

bioRxiv2022

The velvet family proteins mediate low resistance to isoprothiolane in Magnaporthe oryzae

Isoprothiolane (IPT) resistance has emerged in Magnaporthe oryzae, due to the long-term usage of IPT to control rice blast in China, yet the mechanisms of the resistance remain largely unknown. Through IPT adaptation on PDA medium, we obtained a variety of IPT-resistant mutants. Based on their EC50 values to IPT, the resistant mutants were mainly divided into three distinct categories i.e., low resistance (LR, 6.5 [≤] EC50 < 13.0 g/mL), moderate resistance 1 (MR-1, 13.0 [≤] EC50 < 25.0 g/mL), and moderate resistance 2 (MR-2, 25.0 [≤] EC50 < 35.0 g/mL). Molecular analysis of MoIRR (Magnaporthe oryzae isoprothiolane resistance related) gene demonstrated that it was associated only with the moderate resistance in MR-2 mutants, indicating that other mechanisms were associated with resistance in LR and MR-1 mutants. In this study, we mainly focused on the characterization of low resistance to IPT in M. oryzae. Mycelial growth and conidial germination were significantly reduced, indicating fitness penalties in LR mutants. Based on the differences of whole genome sequences between parental isolate and LR mutants, we identified a conserved MoVelB gene, encoding the velvet family transcription factor, and genetic transformation of wild type isolate verified that MoVelB gene was associated with the low resistance. Based on molecular analysis, we further demonstrated that the velvet family proteins VelB and VeA were indispensable for IPT toxicity and the deformation of the LaeA-VeA-VelB heterotrimer played a vital role for the low IPT-resistance in M. oryzae, most likely through the down-regulation of the secondary metabolism-related genes or CYP450 genes to reduce the toxicity of IPT. Author summaryIsoprothiolane (IPT) resistance has emerged in Magnaporthe oryzae, due to the long-term usage of IPT to control rice blast in China, yet the mechanisms of the resistance remain largely unknown. Here, we explored the mechanisms of low IPT resistance in M. oryzae. Combining the whole genome sequencing and genetic transformation, we identified a conserved MoVelB gene, encoding the velvet family transcription factor to be a determinant for IPT toxicity. We further demonstrated that the deformation of the LaeA-VeA-VelB heterotrimer conferred the low IPT-resistance in M. oryzae, most likely through down-regulating the secondary metabolism-related genes or CYP450 genes to reduce the toxicity of IPT. This study improved our understanding of the resistance mechanism as well as the mode of action of IPT which will be helpful for making suitable strategies to manage the emerging resistance of IPT in M. oryzae.

microbiology↗

bioRxiv2022

Upf3a is dispensable for nonsense-mediated mRNA decay in mouse pluripotent and somatic cells

Nonsense-mediated mRNA decay (NMD) is a highly conserved regulatory mechanism of post-transcriptional gene expression in eukaryotic cells. NMD plays essential roles in mRNA quality and quantity control, and thus safeguards multiple biological processes including embryonic stem cell differentiation and organogenesis. UPF3A and UPF3B in vertebrate species, originated from a single UPF3 gene in yeast, are key factors in the NMD machinery. While UPF3B is a well-recognized weak NMD-promoting factor, whether UPF3A functions in promoting or suppressing NMD is under debate. In this study, we generated a Upf3a conditional knockout mouse strain, and established multiple lines of embryonic stem cells and somatic cells without UPF3A. Through extensive analysis on the expressions of 33 NMD targets, we found UPF3A neither represses NMD in mouse embryonic stem cells, somatic cells, nor in major organs including the liver, spleen, and thymus. Our study reinforces that UPF3A is dispensable for NMD when UPF3B is present. Furthermore, UPF3A may weakly and selectively promote NMD in certain murine organs. Summary blurbWe generated a new Upf3a inducible knockout mouse model and showed that UPF3A does not repress expressions of NMD target genes in embryonic stem cells, somatic fibroblasts, as well as multiple tissues from adult mice.

cell biology↗

bioRxiv2020

HetF protein is a new divisome component in a filamentous and developmental cyanobacterium

Bacterial cell division, with a few exceptions, is driven by FtsZ through a treadmilling mechanism to remodel and constrict the rigid peptidoglycan (PG) layer. Yet, different organisms may differ in the composition of the cell-division complex (divisome). In the filamentous cyanobacterium Anabaena PCC 7120, hetF is required for the initiation of the differentiation of heterocysts, cells specialized in N2-fixing cells under combined nitrogen deprivation. In this study, we demonstrate that hetF is expressed in vegetative cells and necessary for cell division in a conditional manner. Under non-permissive conditions, cells of a {Delta}hetF mutant stop dividing, consistent with increased level of HetF under similar conditions in the wild type. Furthermore, HetF is a membrane protein located at midcell and cell-cell junctions. In the absence of HetF, FtsZ rings are still present in the elongated cells; however, PG remodelling is abolished. This phenotype is similar to that observed with the inhibition of septal PG synthase FtsI. We further reveal that HetF is recruited to or stabilized at the divisome by interacting with FtsI and this interaction is necessary for HetF function in cell division. Our results indicate that HetF is a member of the divisome, and reveal distinct features of the cell-division machinery in cyanobacteria that are of high ecological and environmental importance. Significance StatementCyanobacteria shaped the Earths evolutionary history, and are still playing important roles for elementary cycles in different environments. They are consisted of highly diverse species with different cell shape, size and morphology. Although these properties are strongly affected by the process of cytokinesis, the mechanism remains largely unexplored. Using different approaches, we demonstrate that HetF is a new component of the cell division machinery in the filamentous cyanobacterium Anabaena PCC 7120. The common and diverged characteristics of cell division in prokaryotes reflect the evolutionary history of different bacteria, as an adaptive measure to proliferate under certain environmental conditions. As a protein for cell differentiation, the recruitment of HetF to the septum illustrates such an adaptive mechanism for cyanobacteria.

microbiology↗

bioRxiv2019

Function of TRIP6 in brain-specific ciliogenesis

TRIP6, a member of the zyxin-family of LIM domain proteins, is a focal adhesion component. trip6 deletion in the mouse revealed, unexpectedly, in view of its ubiquitous expression, a function in the brain: ependymal and choroid plexus epithelial cells were poorly developed, carrying fewer and shorter cilia, and the mice developed hydrocephalus. TRIP6 disruption, via RNAi or inhibition of its homodimerization, in a choroid plexus epithelial cell line, confirmed its function in ciliogenesis. Zyxin-family members carry numerous protein interaction domains. In common with assembly of other multiprotein complexes, ciliogenesis may be facilitated by molecular assembly factors. Super-resolution microscopy demonstrated TRIP6 localization at the pericentriolar material and along the ciliary axoneme. The requirement for homodimerization which doubles its interaction sites, its punctate localization along the axoneme, and its co-localization with other cilia components suggest a scaffold/co-transporter function for TRIP6 in cilia. This is the first discovery of a protein assembly factor essential for mammalian ciliogenesis.

cell biology↗

bioRxiv2018

Reduced expression of C/EBPβ-LIP extends health- and lifespan in mice

Ageing is associated with physical decline and the development of age-related diseases such as metabolic disorders and cancer. Few conditions are known that attenuate the adverse effects of ageing, including calorie restriction (CR) and reduced signalling through the mechanistic target of rapamycin complex 1 (mTORC1) pathway. Synthesis of the metabolic transcription factor C/EBP {beta} -LIP is stimulated by mTORC1, which critically depends on a short upstream open reading frame (uORF) in the C/EBP {beta}-mRNA. Here we describe that reduced C/EBP {beta} -LIP expression due to genetic ablation of the uORF delays the development of age-associated phenotypes in mice. Moreover, female C/EBP {beta}{Delta}uORF mice display an extended lifespan. Since LIP levels increase upon aging in wt mice, our data reveal an important role for C/EBP{beta} in the aging process and suggest that restriction of LIP expression sustains health and fitness. Thus, therapeutic strategies targeting C/EBP {beta} -LIP may offer new possibilities to treat age-related diseases and to prolong healthspan.

cell biology↗