scholarly journals Transcriptional and epi-transcriptional dynamics of SARS-CoV-2 during cellular infection

Cell Reports ◽  
2021 ◽  
pp. 109108
Author(s):  
Jessie J.-Y. Chang ◽  
Daniel Rawlinson ◽  
Miranda E. Pitt ◽  
George Taiaroa ◽  
Josie Gleeson ◽  
...  
Author(s):  
Sahar Hani ◽  
Laura Cuyas ◽  
Pascale David ◽  
David Secco ◽  
James Whelan ◽  
...  

iScience ◽  
2021 ◽  
pp. 102838
Author(s):  
Yuan Wen ◽  
Davis A. Englund ◽  
Bailey D. Peck ◽  
Kevin A. Murach ◽  
John J. McCarthy ◽  
...  

2021 ◽  
Vol 22 (13) ◽  
pp. 7029
Author(s):  
Cai-Yun Xiong ◽  
Qing-You Gong ◽  
Hu Pei ◽  
Chang-Jian Liao ◽  
Rui-Chun Yang ◽  
...  

In maize, the ear shank is a short branch that connects the ear to the stalk. The length of the ear shank mainly affects the transportation of photosynthetic products to the ear, and also influences the dehydration of the grain by adjusting the tightness of the husks. However, the molecular mechanisms of maize shank elongation have rarely been described. It has been reported that the maize ear shank length is a quantitative trait, but its genetic basis is still unclear. In this study, RNA-seq was performed to explore the transcriptional dynamics and determine the key genes involved in maize shank elongation at four different developmental stages. A total of 8145 differentially expressed genes (DEGs) were identified, including 729 transcription factors (TFs). Some important genes which participate in shank elongation were detected via function annotation and temporal expression pattern analyses, including genes related to signal transduction hormones (auxin, brassinosteroids, gibberellin, etc.), xyloglucan and xyloglucan xyloglucosyl transferase, and transcription factor families. The results provide insights into the genetic architecture of maize ear shanks and developing new varieties with ideal ear shank lengths, enabling adjustments for mechanized harvesting in the future.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yumeko Satou-Kobayashi ◽  
Jun-Dal Kim ◽  
Akiyoshi Fukamizu ◽  
Makoto Asashima

AbstractActivin, a member of the transforming growth factor-β (TGF-β) superfamily of proteins, induces various tissues from the amphibian presumptive ectoderm, called animal cap explants (ACs) in vitro. However, it remains unclear how and to what extent the resulting cells recapitulate in vivo development. To comprehensively understand whether the molecular dynamics during activin-induced ACs differentiation reflect the normal development, we performed time-course transcriptome profiling of Xenopus ACs treated with 50 ng/mL of activin A, which predominantly induced dorsal mesoderm. The number of differentially expressed genes (DEGs) in response to activin A increased over time, and totally 9857 upregulated and 6663 downregulated DEGs were detected. 1861 common upregulated DEGs among all Post_activin samples included several Spemann’s organizer genes. In addition, the temporal transcriptomes were clearly classified into four distinct groups in correspondence with specific features, reflecting stepwise differentiation into mesoderm derivatives, and a decline in the regulation of nuclear envelop and golgi. From the set of early responsive genes, we also identified the suppressor of cytokine signaling 3 (socs3) as a novel activin A-inducible gene. Our transcriptome data provide a framework to elucidate the transcriptional dynamics of activin-driven AC differentiation, reflecting the molecular characteristics of early normal embryogenesis.


2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi213-vi213
Author(s):  
Kevin Joseph ◽  
Lea Vollmer ◽  
Vidyha Ravi ◽  
Jürgen Beck ◽  
Ulrich Hofmann ◽  
...  

Abstract OBJECTIVE Owing to recent advances in understanding of the active functional states exhibited within glioblastoma (GBM), intra-tumoral cellular signaling has moved into focus of neuro-oncology. In this study, we aim to explore the diversity of transcellular signaling and investigate correlations between transcriptional dynamics and functional signaling. METHODS Electrophysiological characterization of GBM was carried out using planar microelectrodes and Ca2+ imaging, in both 2D cell culture as well as in our novel human cortical GBM model. Exposure to physiologically relevant conditions present within the tumor was carried out to identify specific signaling cells of interest and capture the signaling diversity in response to environmental conditions. Transcriptional dynamics and plasticity were examined by means of scRNA-sequencing with CRISPR based perturbation, spatial transcriptomics and deep long-read RNA-sequencing. RESULTS Electrophysiological profiles of multiple primary GBM cell lines revealed characteristics of scale-free networks (R2=0.875), confirmed in both 2D culture as well as a human neocortical GBM model. When GBM was cultured in a “in-vivo” like environment, basal activity was significantly higher (50%, p=0.01). Cellular signaling was directly correlated to changes in the environment, like hypoxia or glutamatergic activation, and total inhibition of electrical signaling required the usage of synaptic inhibitors. Using single-cell RNA sequencing and proteomics, several synaptogenesis related genes were identified to play a crucial role in the lineage states present in GBM. CRISPR based perturbation of these genes resulted in alterations in cellular morphology and decreased cellular connectivity (p< 0.01), with loss of scale free features (R2=0.35), and transcriptomic loss of developmental lineages (FDR< 0.01), leading to significant inhibition of GBM stress response. CONCLUSION Our findings highlight the role of electrical signaling in glioblastoma. Cellular stressors induce intercellular signaling, leading to transcriptional adaptation suggesting that there exists a highly complex and powerful mechanism for dynamic transcriptional state adaptation.


Science ◽  
2018 ◽  
Vol 361 (6409) ◽  
pp. 1341-1345 ◽  
Author(s):  
Eileen E. M. Furlong ◽  
Michael Levine

Developmental enhancers mediate on/off patterns of gene expression in specific cell types at particular stages during metazoan embryogenesis. They typically integrate multiple signals and regulatory determinants to achieve precise spatiotemporal expression. Such enhancers can map quite far—one megabase or more—from the genes they regulate. How remote enhancers relay regulatory information to their target promoters is one of the central mysteries of genome organization and function. A variety of contrasting mechanisms have been proposed over the years, including enhancer tracking, linking, looping, and mobilization to transcription factories. We argue that extreme versions of these mechanisms cannot account for the transcriptional dynamics and precision seen in living cells, tissues, and embryos. We describe emerging evidence for dynamic three-dimensional hubs that combine different elements of the classical models.


2019 ◽  
Vol 25 (1) ◽  
pp. 87-102.e9 ◽  
Author(s):  
Nicole R. Stone ◽  
Casey A. Gifford ◽  
Reuben Thomas ◽  
Karishma J.B. Pratt ◽  
Kaitlen Samse-Knapp ◽  
...  

2020 ◽  
Vol 6 (6) ◽  
pp. eaay5247 ◽  
Author(s):  
Haohuan Xie ◽  
Wen Zhang ◽  
Mei Zhang ◽  
Tasneem Akhtar ◽  
Young Li ◽  
...  

Retinal organoids (ROs) derived from human induced pluripotent stem cells (hiPSCs) provide potential opportunities for studying human retinal development and disorders; however, to what extent ROs recapitulate the epigenetic features of human retinal development is unknown. In this study, we systematically profiled chromatin accessibility and transcriptional dynamics over long-term human retinal and RO development. Our results showed that ROs recapitulated the human retinogenesis to a great extent, but divergent chromatin features were also discovered. We further reconstructed the transcriptional regulatory network governing human and RO retinogenesis in vivo. Notably, NFIB and THRA were identified as regulators in human retinal development. The chromatin modifications between developing human and mouse retina were also cross-analyzed. Notably, we revealed an enriched bivalent modification of H3K4me3 and H3K27me3 in human but not in murine retinogenesis, suggesting a more dedicated epigenetic regulation on human genome.


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