Search bioRxiv⌕ Search

bioRxiv · 10.1101/2023.01.14.524062

Temporal physiological, transcriptomic and metabolomic analyses revealed molecular mechanism of Canna indica's response to Cr stress

Abstract

Chromium (Cr) can interfere with plant gene expression, change the content of metabolites and affect plant growth. However, the molecular response mechanism of wetland plants at different time sequences under Cr stress has yet to be fully understood.The results showed that Cr stress increased the activities of superoxide dismutase (SOD), ascorbate peroxidase (APX) and peroxidase (POD), the contents of glutathione (GSH), malondialdehyde (MDA), and oxygen free radical (ROS), and inhibited the biosynthesis of photosynthetic pigments, thus leading to changes in plant growth and biomass. that Cr stress mainly affected 12 metabolic pathways, involving 38 differentially expressed metabolites, including amino acids, phenylpropane, and flavonoids. A total of 16247 differentially expressed genes were identified, among which, at the early stage of stress, C. indica responds to Cr toxicity mainly through galactose, starch and sucrose metabolism. With the extension of stress time, plant hormone signal transduction and MAPK signaling pathway in C. indica in the treatment group were significantly affected. Finally, in the late stage of stress, C. indica co-defuses Cr toxicity by activating its Glutathione metabolism and Phenylpropanoid biosynthesis. In conclusion, this study revealed the molecular response mechanism of C. indica to Cr stress at different times through multi-omics methods. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=118 SRC="FIGDIR/small/524062v1_ufig1.gif" ALT="Figure 1"> View larger version (36K): org.highwire.dtl.DTLVardef@c2fec6org.highwire.dtl.DTLVardef@1e47da8org.highwire.dtl.DTLVardef@1f5be49org.highwire.dtl.DTLVardef@9fcf87_HPS_FORMAT_FIGEXP M_FIG C_FIG

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Wei, Z., Zhongbing, C., Xiuqing, Y., Luying, S., Huan, M., Sixi, Z.. 2023-01-17. Temporal physiological, transcriptomic and metabolomic analyses revealed molecular mechanism of Canna indica's response to Cr stress. https://doi.org/10.1101/2023.01.14.524062

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Trans-branching of polyubiquitin chains orchestrates the DNA replication stress response

Polyubiquitin chain geometry dictates functional consequences of ubiquitylation. Although branched polyubiquitin chains are abundant in cells, little is known about their functions. Here we show that branching on the DNA replication factor PCNA, mediated by the ubiquitin-conjugating enzyme UBE2K and involving lysines 63 and 48 of ubiquitin, orchestrates the sequence of events in response to replication stress. By inducing VCP-dependent extraction of PCNA from chromatin, branching promotes re-priming of stalled forks and necessitates a BRCA1-dependent pathway of daughter-strand gap repair. Our study identifies hyper-accumulation of daughter-strand gaps as the mechanistic basis underlying the toxicity of inhibitors of the PCNA-specific isopeptidase, USP1, in BRCA1-deficient cells. Moreover, an unexpected preference of UBE2K to operate in trans suggests a general timing mechanism to organize hierarchies amongst ubiquitin signals.

molecular biology↗

Impaired proteostasis is an early feature of the diabetic heart in humans and mice

Diabetes and obesity increase cardiac lipid levels leading to cardiomyopathy and heart failure. We hypothesized that intermittent fasting would reduce cardiac lipid levels. Surprisingly, intermittent fasting increased myocardial triglyceride content, but rescued mortality and attenuated cardiomyopathy in mice overexpressing cardiomyocyte acyl-CoA synthetase 1 (MHC-ACSL1). Lipid overload caused cardiomyocyte accumulation of polyubiquitinated protein aggregates containing desmin, a scaffolding intermediate filament protein, which intermittent fasting prevented. Furthermore, intermittent fasting reversed elevated myocardial C16:0 ceramide content, and knockdown of ceramide synthase CerS5 and CerS6 reduced palmitate-induced protein aggregation, highlighting a role for C16:0 ceramides in this pathology. Conversely, impairing aggrephagy with cardiomyocyte-specific p62 ablation induced heart failure in mice fed a high-fat diet, with paradoxically reduced cardiac lipid content. Crucially, non-failing diabetic human hearts also exhibited protein aggregate pathology. Taken together, these results demonstrate that impaired proteostasis characterizes cardiomyopathy from cardiac lipid overload and identify a promising new therapeutic target for this condition.

molecular biology↗

Spatial profiling and neurovascular communication in the developing and adolescent cortex following prenatal alcohol exposure

Fetal alcohol spectrum disorders (FASD) constitute a wide range of developmental, cognitive, and behavioral impairments caused by prenatal alcohol exposure (PAE). Although neuronal and vascular consequences of PAE have been studied, how alcohol affects the cerebrovasculature within the framework of the neurovascular unit (NVU) across development remains poorly understood. At minimum, the NVU comprises neurons, astrocyte endfeet, and endothelial cells (ECs), which coordinate to maintain brain homeostasis. Here, we used the NanoString Digital Spatial Profiling platform to characterize spatial transcriptomic data from neurons, astrocytes, and ECs from PAE and saccharin (SAC) control cortices at embryonic day 18 (E18) and postnatal day 28 (P28). Differentially expressed genes were then used for Ingenuity Pathway Analysis (IPA) to identify altered biological pathways and perform comparison analyses across developmental time points, while CellChat was used to infer cell cell communication networks. We uncovered thousands of differentially expressed genes and numerous altered pathways and biological processes in PAE cortices across development. Both IPA and CellChat analyses implicated dysregulation of vascular and extracellular matrix (ECM) remodeling, cell adhesion, and neuroinflammatory signaling. CellChat further predicted the loss of several key bidirectional relationships and altered ligand-receptor interactions among neurovascular cell types at E18 and P28. Overall, these findings identify PAE associated alterations in neurovascular gene expression and intercellular signaling across development, providing potential mechanisms by which PAE may disrupt neurodevelopment.

molecular biology↗