Highlights to be read in the October 2020 issue of Cell

October 31, 2020 / --- October 2020 is coming to an end, what are the highlights of the October Cell journal research worth learning? The editor-in-chief has organized this and shared it with you.
1.Cell: Great progress! β in a new study, researchers from the National Institutes of Health (NIH) have found a biological pathway that they appear to be able to use when the β coronavirus, including SARS-CoV-2, spreads in the body using lysosomes to hijack and leave infected cells doi:10.1016/j.cell.2020.10.039 In a new study, researchers from the National Institutes of Health (NIH) have found a biological pathway through which β coronavirus, including SARS-CoV-2, can be transmitted in the body.
understanding of this important pathway may provide important new insights in preventing the spread of the SARS-CoV-2 coronavirus, which causes COVID-19 disease.
results were published online October 27, 2020 in the journal Cell under the title "β-Coronaviruses use lysosomes for egress of the biosynthetic pathway."
from Cell, 2020, doi:10.1016/j.cell.2020.10.039.
in cell studies, the authors found for the first time that β coronavirus can leave infected cells through lysosomes --- a cell device called a cell "junk compactor---
, lysosomes experience destroying viruses and other pathogens before they leave the cells.
, however, the authors found that β coronavirus infests the lysosome's disease-resistant mechanisms, allowing it to spread freely in the body.
targeting this lysosome pathway could lead to the development of new and more effective antiviral therapies to combat COVID-19.
2.Cell: Identification of genes and drug targets against new coronavirus infections through CRISPR screening doi:10.1016/j.cell.2020.10.030 in one In the new study, researchers from research institutions such as New York University, the New York Genomics Center and mount Sinai's Icahn School of Medicine conducted genome-wide functional absence CRISPR screening to systematically knock out genes from the human genome.
they studied which genetic modifications make human lung cells more resistant to SARS-CoV-2 infections.
their findings shed light on which genes and gene regulatory networks in the human genome are needed for SARS-CoV-2 infections, suppressing the genes that give them resistance to the coronavirus infection.
described a series of genes that had not previously been considered targets for SARS-CoV-2 treatments.
study was recently published in the Journal of Cell under the title "Finding of required host factors for SARS-CoV-2 infected in human cells".
to better understand the complex relationship between host and viral genetic dependence, the authors used a series of analytical and experimental methods to verify their results.
methods include genome editing, single-cell sequencing, common focus imaging, and computational analysis of gene expression and proteomic data sets.
they found that these new gene targets, inhibited by the use of small molecules (drugs), significantly reduced viral load, some of which reduced viral load by up to 1,000 times.
their findings provide important insights into the possible development of new drugs for the effective treatment of COVID-19 and reveal their molecular targets.
3.Cell: Genome-wide CRISPR screening identifies host factors that are critical to new coronavirus infections doi:10.1016/j.cell.2020.10.028 In a new study, Yale University in the United States Researchers at research institutions such as the Broad Institute screened hundreds of millions of cells exposed to SARS-CoV-2 and MERS-CoV coronavirus to identify dozens of genes that allow the two viruses to replicate in cells, as well as genes that appear to inhibit them.
say the virus-promoting and antiviral effects of these genes will help guide scientists in developing new therapies to fight COVID-19.
study was recently published in the Journal of Cell under the title "Genome-wide CRISPR screens reveal host factors critical for SARS-CoV-2 infect".
image from the NIH.
the new study, the researchers screened green monkey cells for whole-genome CRISPR, in which they were more likely to die after exposure to SARS-CoV-2 than commonly used human cell line.
screening allows them to track both virus and cell interactions.
screening confirms earlier findings that the ACE-2 gene, which encodes cell surface receptors, promotes SARS-CoV-2 infection of host cells.
, however, the screening also found two new viral protein complexes and a third protein complex that appears to help prevent infection.
found that SWI/SNF complexes that turn genes on and off and HMGB1, which has many functions, including regulating inflammation, were associated with increased cell death after infection.
the researchers then added small molecule drugs that inhibited the function of the two gene products that had been found, and found that they could increase the survival of cells in petri dishes after infection.
, the histoprotein H3 complex, which helps regulate gene expression in the nuclei of cells, appears to provide a protective effect that inhibits THES-CoV-2's ability to infect and kill cells.
4.Cell interpretation! Can scientists really use CRISPR/Cas9 technology to correct mutations in human embryos? Maybe it's too early! image from Cell, 2020, doi:10.1016/j.cell.2020.09.022.
Sperandio team found that raising the level of 2-AG could also reduce salmonella infection in mice and prevent E. coli, a particularly dangerous gastrointestinal bacterium that infects humans, from expressing the toxic characteristics needed for a successful infection.
, when the researchers treated mammalian cells in petri dishes with tetrahydrolipstatin, they became more susceptible to bacterial pathogens.
is a compound approved by the U.S. Food and Drug Administration (FDA) and sold on the market under the name Alli.
7.Cell: Our scientists have revealed the pathogenesis of Noonan syndrome and multiple freckle Nounan syndrome doi:10.1016/j.cell.2020.09.002 Noonan syndrome (Noonan syndrome, NS) and multiple freckle nounan syndrome (Noonan syndrome with multiple).