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"Zhang, Zhong"
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The royal bee
In the days when only wealthy Korean children are allowed to attend school, a poor boy named Song-ho learns by listening outside a schoolroom door, which eventually earns him a chance to better himself and make life easier for his widowed mother.
Book
Genome Wide Analysis of the Apple MYB Transcription Factor Family Allows the Identification of MdoMYB121 Gene Confering Abiotic Stress Tolerance in Plants
The MYB proteins comprise one of the largest families of transcription factors (TFs) in plants. Although several MYB genes have been characterized to play roles in secondary metabolism, the MYB family has not yet been identified in apple. In this study, 229 apple MYB genes were identified through a genome-wide analysis and divided into 45 subgroups. A computational analysis was conducted using the apple genomic database to yield a complete overview of the MYB family, including the intron-exon organizations, the sequence features of the MYB DNA-binding domains, the carboxy-terminal motifs, and the chromosomal locations. Subsequently, the expression of 18 MYB genes, including 12 were chosen from stress-related subgroups, while another 6 ones from other subgroups, in response to various abiotic stresses was examined. It was found that several of these MYB genes, particularly MdoMYB121, were induced by multiple stresses. The MdoMYB121 was then further functionally characterized. Its predicted protein was found to be localized in the nucleus. A transgenic analysis indicated that the overexpression of the MdoMYB121 gene remarkably enhanced the tolerance to high salinity, drought, and cold stresses in transgenic tomato and apple plants. Our results indicate that the MYB genes are highly conserved in plant species and that MdoMYB121 can be used as a target gene in genetic engineering approaches to improve the tolerance of plants to multiple abiotic stresses.
Journal Article
هذه هي الصين : قوة تسير نحو العالم
يركز كتاب \"هذه هي الصين\" على سرد قصص تنمية الصين في العصر الجديد. وقد غير الدكتور تشانغ وي وي طريقته المعروفة بالتوجيه والإرشاد في البرامج الأيديولوجية والنظرية في الماضي، وعبر عنها بلغة شعبية سائغة، وحجج منطقية صارمة، وبيانات حقيقية، وتصادمات صريحة للأفكار، وتقنيات عرض مبتكرة لمساعدة الجمهور على فهم النموذج الصيني والطريق الصيني، وتعزيز ثقتهم بمستقبل الصين.
Book
Pathogenicity and Complete Genome Characterization of Fowl Adenoviruses Isolated from Chickens Associated with Inclusion Body Hepatitis and Hydropericardium Syndrome in China
In this study, we determined and genetically characterized three fowl adenoviruses isolated from chickens with inclusion body hepatitis (IBH) and hydropericardium syndrome (HPS) in China and assessed their pathogenicity. The full genome of HBQ12, BJH13 and JSJ13 was found to be 44,081, 43,966 and 43,756 nucleotides long, respectively. Sequence alignment and phylogenetic analysis revealed that strain HBQ12 and BJH13 were clustered together belonging to fowl adenoviruses D species and serotyped as FAdV-11, whereas strain JSJ13 was classified into fowl adenoviruses C species and serotyped as FAdV-4. To our knowledge, this is the first report of FAdV-4 strain circulating in China. The pathogenicity test showed that mortality for chickens infected with HBQ12 and JSJ13 within 21 days post infection (dpi) was 8.6% and 28.6%, respectively. Necropsy displayed mild or severe hepatitis and hydropericardium at 3 and 5 dpi as well as dead chickens. Viral DNA was detected in almost all tissues sampled from dead chickens. These results revealed that fowl adenovirus strains HBQ12 and JSJ13 are capable of causing IBH and HPS in chickens, indicating that preventive measures against FAdV infection on poultry farms should be implemented in China.
Journal Article
Protein tyrosine phosphatases as potential therapeutic targets
Protein tyrosine phosphorylation is a key regulatory process in virtually all aspects of cellular functions. Dysregulation of protein tyrosine phosphorylation is a major cause of human diseases, such as cancers, diabetes, autoimmune disorders, and neurological diseases. Indeed, protein tyrosine phosphorylation-mediated signaling events offer ample therapeutic targets, and drug discovery efforts to date have brought over two dozen kinase inhibitors to the clinic. Accordingly, protein tyrosine phosphatases （PTPs） are considered next-generation drug targets. For instance, PTPIB is a well-known targets of type 2 diabetes and obesity, and recent studies indicate that it is also a promising target for breast cancer. SHP2 is a bona-fide oncoprotein, mutations of which cause juvenile myelomonocytic leukemia, acute myeloid leukemia, and solid tumors. In addition, LYP is strongly associated with type I diabetes and many other autoimmune diseases. This review summarizes recent findings on several highly recognized PTP family drug targets, including PTPIB, Src homology phosphotyrosyl phosphatase 2 （SHP2）, lymphoid-specific tyrosine phosphatase （LYP）, CD45, Fas associated phosphatase-1 （FAP-1）, striatal enriched tyrosine phosphatases （STEP）, mitogen-activated protein kinase/dual-specificity phosphatase 1 （MKP-1）, phosphatases of regenerating liver-1 （PRL）, low molecular weight PTPs （LMWPTP）, and CDC25. Given that there are over 100 family members, we hope this review will serve as a road map for innovative drug discovery targeting PTPs.
Journal Article
Thrombin induces ACSL4-dependent ferroptosis during cerebral ischemia/reperfusion
Ischemic stroke represents a significant danger to human beings, especially the elderly. Interventions are only available to remove the clot, and the mechanism of neuronal death during ischemic stroke is still in debate. Ferroptosis is increasingly appreciated as a mechanism of cell death after ischemia in various organs. Here we report that the serine protease, thrombin, instigates ferroptotic signaling by promoting arachidonic acid mobilization and subsequent esterification by the ferroptotic gene, acyl-CoA synthetase long-chain family member 4 (ACSL4). An unbiased multi-omics approach identified thrombin and ACSL4 genes/proteins, and their pro-ferroptotic phosphatidylethanolamine lipid products, as prominently altered upon the middle cerebral artery occlusion in rodents. Genetically or pharmacologically inhibiting multiple points in this pathway attenuated outcomes of models of ischemia in vitro and in vivo. Therefore, the thrombin-ACSL4 axis may be a key therapeutic target to ameliorate ferroptotic neuronal injury during ischemic stroke.
Journal Article
Cyanobacteria blooms induced precipitation of calcium carbonate and dissolution of silica in a subtropical lagoon, Florida Bay, USA
In recent decades, annual cyanobacteria blooms in Florida Bay displayed spatial and temporal patterns that are consistent with changes in alkalinity and dissolved silicon in water. In early summer, the blooms developed in the north–central bay and spread southward in fall. The blooms drew down dissolved inorganic carbon and increased water pH, causing in situ precipitation of calcium carbonate. Dissolved silicon concentrations in these waters were at minimum in spring (20–60 µM), increased during summer, and reached an annual maximum (100–200 µM) during late summer. The dissolution of silica as a result of high pH in bloom water was first observed in this study. During the peak of blooms, silica dissolution in Florida Bay varied from 0.9 × 10
7
to 6.9 × 10
7
mol per month over the study period, depending on the extent of cyanobacteria blooms in a given year. Concurrent calcium carbonate precipitations in the cyanobacteria bloom region are between 0.9 × 10
8
and 2.6 × 10
8
mol per month. It is estimated that 30–70% of atmospheric CO
2
uptake in bloom waters was precipitated as calcium carbonate mineral and remainders of CO
2
influx were used for the production of biomass.
Journal Article
Whole chromosome loss and genomic instability in mouse embryos after CRISPR-Cas9 genome editing
Karyotype alterations have emerged as on-target complications from CRISPR-Cas9 genome editing. However, the events that lead to these karyotypic changes in embryos after Cas9-treatment remain unknown. Here, using imaging and single-cell genome sequencing of 8-cell stage embryos, we track both spontaneous and Cas9-induced karyotype aberrations through the first three divisions of embryonic development. We observe the generation of abnormal structures of the nucleus that arise as a consequence of errors in mitosis, including micronuclei and chromosome bridges, and determine their contribution to common karyotype aberrations including whole chromosome loss that has been recently reported after editing in embryos. Together, these data demonstrate that Cas9-mediated germline genome editing can lead to unwanted on-target side effects, including major chromosome structural alterations that can be propagated over several divisions of embryonic development.
A possible undesired outcome of CRISPR-Cas9 germline editing is unwanted karyotype alterations. Here the authors track aberrations through three divisions of embryonic development following Cas9 editing.
Journal Article
Attenuated replication and pathogenicity of SARS-CoV-2 B.1.1.529 Omicron
The Omicron (B.1.1.529) variant of SARS-CoV-2 emerged in November 2021 and is rapidly spreading among the human population
1
. Although recent reports reveal that the Omicron variant robustly escapes vaccine-associated and therapeutic neutralization antibodies
2
–
10
, the pathogenicity of the virus remains unknown. Here we show that the replication of Omicron is substantially attenuated in human Calu3 and Caco2 cells. Further mechanistic investigations reveal that Omicron is inefficient in its use of transmembrane serine protease 2 (TMPRSS2) compared with wild-type SARS-CoV-2 (HKU-001a) and previous variants, which may explain its reduced replication in Calu3 and Caco2 cells. The replication of Omicron is markedly attenuated in both the upper and lower respiratory tracts of infected K18-hACE2 mice compared with that of the wild-type strain and Delta (B.1.617.2) variant, resulting in its substantially ameliorated lung pathology. Compared with wild-type SARS-CoV-2 and the Alpha (B.1.1.7), Beta (1.351) and Delta variants, infection by Omicron causes the lowest reduction in body weight and the lowest mortality rate. Overall, our study demonstrates that the replication and pathogenicity of the Omicron variant of SARS-CoV-2 in mice is attenuated compared with the wild-type strain and other variants.
The replication and pathogenicity of the Omicron variant of SARS-CoV-2 is attenuated compared with the original strain and other variants.
Journal Article
Chromothripsis as an on-target consequence of CRISPR–Cas9 genome editing
Genome editing has therapeutic potential for treating genetic diseases and cancer. However, the currently most practicable approaches rely on the generation of DNA double-strand breaks (DSBs), which can give rise to a poorly characterized spectrum of chromosome structural abnormalities. Here, using model cells and single-cell whole-genome sequencing, as well as by editing at a clinically relevant locus in clinically relevant cells, we show that CRISPR–Cas9 editing generates structural defects of the nucleus, micronuclei and chromosome bridges, which initiate a mutational process called chromothripsis. Chromothripsis is extensive chromosome rearrangement restricted to one or a few chromosomes that can cause human congenital disease and cancer. These results demonstrate that chromothripsis is a previously unappreciated on-target consequence of CRISPR–Cas9-generated DSBs. As genome editing is implemented in the clinic, the potential for extensive chromosomal rearrangements should be considered and monitored.
Chromothripsis, a chromosomal shattering event, can be elicited by micronuclei and chromosome bridges formed by CRISPR–Cas9-generated double-stranded breaks. Extensive chromosomal rearrangements may thus be an on-target effect of genome editing.
Journal Article