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The CRISPR/Cas revolution continues: From efficient gene editing for crop breeding to plant synthetic biology

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Journal of Integrative Plant biology 2018年第12期60卷 1127-1153页

作者： Jochen Kumlehn Janine Pietralla Goetz Hensel Michael Pacher Holger Puchta Plant Reproductive biology Leibniz Institute of Plant Genetics and Crop Plant Research (IPK) Botanical institute Molecular Biology and Biochemistry Karlsruhe Institute of Technology

Since the discovery that nucleases of the bacterial CRISPR(clustered regularly interspaced palindromic repeat)-associated(Cas) system can be used as easily programmable tools for genome engineering,their application massively transformed different areas of plant biology. In this review, we assess the current state of their use for crop breeding to incorporate attractive new agronomical traits into specific cultivars of various crop plants. This can be achieved by the use of Cas9/12 nucleases for double-strand break induction,resulting in mutations by non-homologous recombinatr e-tion. Strategies for performing such experiments à from Rthe design of guide RNA to the use of different transformation technologies à are evaluated. Furtherweive-more, we sum up recent developments regarding the use of nuclease-deficient Cas9/12 proteins, as DNAbinding moieties for targeting different kinds of enzyme activities to specific sites within the genome. Progress in base deamination, transcriptional induction and transcriptional repression, as well as in imaging in plants, is also discussed. As different Cas9/12 enzymes are at hand, the simultaneous application of various enzyme activities, to multiple genomic sites, is now in reach to redirect plant metabolism in a multifunctional manner and pave the way for a new level of plant synthetic biology.

关键词： From efficient gene editing for crop breeding to plant synthetic biology The CRISPR/Cas revolution continues

DNA End Resection:Facts and Mechanisms

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Genomics, Proteomics & Bioinformatics 2016年第3期14卷 126-130页

作者： Ting Liu Jun Huang Department of Cell biology and Program in molecular Cell biology Zhejiang University School of Medicine Life Sciences institute and Innovation Center for Cell Signaling Network Zhejiang University

DNA double-strand breaks（DSBs）,which arise following exposure to a number of endogenous and exogenous agents,can be repaired by either the homologous recombination（HR）or non-homologous end-joining（NHEJ） pathways in eukaryotic cells.A vital step in HR repair is DNA end resection,which generates a long 30single-stranded DNA（ss DNA） tail that can invade the homologous DNA *** generation of 30 ss DNA is not only essential for HR repair,but also promotes activation of the ataxia telangiectasia and Rad3-related protein（ATR）.Multiple factors,including the MRN/X complex,C-terminal-binding protein interacting protein（Ct IP）/Sae2,exonuclease 1（EXO1）,Bloom syndrome protein（BLM）/Sgs1,DNA2 nuclease/helicase,and several chromatin remodelers,cooperate to complete the process of end *** we review the basic machinery involved in DNA end resection in eukaryotic cells.

关键词： DNA end resection Homologous recombination DNA double-strand breaks Chromatin remodeling factors Genome stability

Common genetic variants in the TP53 pathway and their impact on cancer

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Journal of molecular Cell biology 2019年第7期11卷 578-585页

作者： Thibaut Barnoud Joshua L.D.Parris Maureen E.Murphy Program in molecular and Cellular Oncogenesis The Wistar InstitutePhiladelphiaPA 19104USA Cell and molecular biology Program Perelman School of Medicine at the University of PennsylvaniaPhiladelphiaPA 19104USA

The TP53 gene is well known to be the most frequently mutated gene in human *** addition to mutations,there are > 20 different coding region single-nucleotide polymorphisms (SNPs) in the TP53 gene,as well as SNPs in MDM2,the negative regulator of *** of these SNPs are known to alter p53 pathway *** makes p53 rather unique among cancer-critical genes,*** coding regions of other cancer-critical genes like Ha-Ras,RB,and PI3KCA do not have non-synonymous coding region SNPs that alter their function in *** next frontier in p53 biology will consist of probing which of these coding region SNPs are moderately or strongly pathogenic and whether they influence cancer risk and the efficacy of cancer *** challenge after that will consist of determining whether we can tailor chemotherapy to correct the defects for each ofthese *** we review the SNPs in TP53 and MDM2 that show the most significant impact on cancer and other *** also propose avenues for how this information can be used to better inform personalized medicine approaches to cancer and other diseases.

关键词： p53 Pro47Ser Pro72Arg PAS MDM2 SNP309

Spontaneous high-frequency action potential

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Science China(Life Sciences) 2011年第4期54卷 311-335页

作者： Wonchae CHOE Department of Biochemistry and molecular biology Medical Research Center and Biomedical Science InstituteSchool of MedicineKyung Hee University

Action potential,which is the foundation of physiology and electrophysiology,is most vital in physiological *** work starts by detecting cardiac electrophysiology(tachyarrhythmias),combined with all spontaneous discharge phenomena in vivo such as wound currents and spontaneous neuropathic pain,elaborates from generation,induction,initiation,to all of the features of spontaneous high-frequency action potential--SSL action potential mechanism,i.e.,connecting-end hyperpolarization initiates spontaneous depolarization and action potential in somatic *** work resolves the conundrums of in vivo spontaneous discharge in tachyarrhythmias,wounds,denervation supersensitivity,neurogenic pain(hyperalgesia and allodynia),epileptic discharge and diabetic pain in pathophysiological and clinical researches that have puzzled people for a hundred years.

关键词： action potential spontaneous high-frequency action potential tachyarrhythmias atrial fibrillation wound denervation supersensitivity neurogenic pain hyperalgesia and allodynia epileptic discharge diabetic pain regeneration and development

Curcumin reverses T cell-mediated adaptive immune dysfunctions in tumor-bearing hosts

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Cellular & molecular Immunology 2010年第4期7卷 306-315页

作者： Sankar Bhattacharyya Dewan Md Sakib Hossain Suchismita Mohanty Gouri Sankar Sen Sreya Chattopadhyay Shuvomoy Banerjee Juni Chakraborty Kaushik Das Diptendra Sarkar Tanya Das Gaurisankar Sa Division of molecular medicine Bose InstituteKolkataIndia

Immune dysfunction is well documented during tumor progression and likely contributes to tumor immune ***81 cytotoxic T lymphocytes(CTLs)are involved in antigen-specific tumor destruction and CD41 T cells are essential for helping this CD81 T cell-dependent tumor *** often target and inhibit T-cell function to escape from immune *** dysfunction includes loss of effector and memory T cells,bias towards type 2 cytokines and expansion of T regulatory(Treg)*** has previously been shown to have antitumor activity and some research has addressed the immunoprotective potential of this plant-derived polyphenol in tumor-bearing *** we examined the role of curcumin in the prevention of tumor-induced dysfunction of T cell-based immune *** observed severe loss of both effector and memory T-cell populations,downregulation of type 1 and upregulation of type 2 immune responses and decreased proliferation of effector T cells in the presence of ***,in turn,prevented this loss of T cells,expanded central memory T cell(TCM)/effector memory T cell(TEM)populations,reversed the type 2 immune bias and attenuated the tumor-induced inhibition of T-cell proliferation in tumor-bearing *** investigation revealed that tumor burden upregulated Treg cell populations and stimulated the production of the immunosuppressive cytokines transforming growth factor(TGF)-b and IL-10 in these ***,however,inhibited the suppressive activity of Treg cells by downregulating the production of TGF-b and IL-10 in these *** importantly,curcumin treatment enhanced the ability of effector T cells to kill cancer ***,our observations suggest that the unique properties of curcumin may be exploited for successful attenuation of tumor-induced suppression of cell-mediated immune responses.

关键词： CD41/CD81 T cell Effector T cell T-regulatory cell FoxP3 Th1/Th2

Application of CRISPR/Cas-mediated base editing for directed protein evolution in plants

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Science China(Life Sciences) 2020年第4期63卷 613-616页

作者： Niklas Capdeville Patrick Schindele Holger Puchta Botanical institute Molecular Biology and BiochemistryKarlsruhe Institute of TechnologyKarlsruhe 76131Germany

Breeding for improved cultivars of existing crops depends mainly on the available amount of genetic variability in yield or quality related *** thousands of years,humans have relied on naturally occurring mutations to recombine and select improved *** chemical or physical mutagens,the amount and range of mutations could be increased,accelerating the development of new ***,naturally occurring or randomly induced mutations lead to unpredictable breeding outcomes and therefore necessitate tedious rounds of backcrossing to eventually produce useful phenotypes(Pacher and Puchta,2017).

关键词： breeding crops cultivar

Effects of La^(3+) on inward K^+ channels at plasma membr in guard cells

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Science China Chemistry 2005年第2期48卷 143-147页

作者： XUE Shaowu YANG Pin institute of molecular Science Chemical Biology and Molecular Engineering Laboratory of Ministry of Education Shanxi University Taiyuan 030006 China Institute of Molecular Science Chemical Biology and Molecular Engineering Laboratory of Ministry of Education Shanxi University Taiyuan 030006 China

The effects of La3+ on inward K+ channels at plasma membrane in vicia guard cells are investigated using the whole-cell patch-clamp recording mode. It is shown that La3+ on both sides of plasma membrane blocks inward K+ currents in a concentration- dependent manner, indicating that La3+ binding sites may exist on both sides of plasma membrane in guard cells in vicia. The dose response is fitted by the Michaelis-Menten relation characterized by an inhibitor constant Ki of 2.56±0.25 μmol·L?1 (outside membrane) and (1.18±0.11)×10?15 mol·L?1 (inside membrane). Intracellular La3+ has much stronger inhibitory effect on inward K+ currents than ex- tracellular La3+ does, suggesting there may exist stronger binding sites inside membrane than outside membrane. Since ion channel activities of guard cells directly affect plant stomatal movement and water status, our results imply that rare earth elements might have potential practical values in regulating plant water status and strengthening plant drought endurance.

关键词： whole-cell patch-clamp, guard cell, stomatal movements, inward K+ channels, La3+.

Complement genetics,deficiencies,and disease associations

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Protein & Cell 2012年第7期3卷 487-496页

作者： Karine R.Mayilyan institute of molecular biology Armenian National Academy SciencesYerevan 0014Armenia

The complement system is a key component of innate *** than 45 genes encoding the proteins of complement components or their isotypes and subu-nits,receptors,and regulators have been *** genes are distributed throughout different chro-mosomes,with 19 genes comprising three significant complement gene clusters in the human ***-netic deficiency of any early component of the classical pathway(C1q,C1r/s,C2,C4,and C3)is associated with autoimmune diseases due to the failure of clearance of immune complexes(IC)and apoptotic materials,and the impairment of normal humoral ***-cies of mannan-binding lectin(MBL)and the early components of the alternative(factor D,properdin)and terminal pathways(from C3 onward components:C5,C6,C7,C8,C9)increase susceptibility to infections and their *** the association of MBL defi-ciency with a number of autoimmune and infectious disorders has been well established,the effects of the deficiency of other lectin pathway components(ficolins,MASPs)have been less extensively investigated due to our incomplete knowledge of the genetic background of such deficiencies and the functional activity of those *** complement regulators and receptors,the consequences of their genetic deficiency vary de-pending on their specific involvement in the regulatory or signalling steps within the complement cascade and *** article reviews current knowledge and concepts about the genetic load of complement com-ponent deficiencies and their association with *** integrative presentation of genetic data with the latest updates provides a background to further inves-tigations of the disease association investigations of the complement system from the perspective of sys-tems biology and systems genetics.

关键词： complement system deficiency disease association HLA-III RCA

Dying by fire: noncanonical functions of autophagy proteins in neuroinflammation and neurodegeneration

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Neural Regeneration Research 2022年第2期17卷 246-250页

作者： Alexis D.Rickman Addison Hilyard Bradlee L.Heckmann Department of Cell biology Microbiology&Molecular Biology University of South FloridaTampaFLUSA USF Health Byrd Alzheimer’s Center and Neuroscience institute Morsani College of MedicineTampaFLUSA Department of molecular medicine Morsani College of MedicineTampaFLUSA

Neuroinflammation and neurodegeneration are key components in the establishment and progression of neurodegenerative diseases including Alzheimer's Disease(AD). Over the past decade increasing evidence is emerging for the use of components of the canonical autophagy machinery in pathways that are characterized by LC3 lipidation yet are distinct from traditional macro-autophagy. One such pathway that utilizes components of the autophagy machinery to target LC3 to endosomes, a process termed LC3-associated endocytosis(LANDO), has recently been identified and regulates neuroinflammation. Abrogation of LANDO in microglia cells results in a propensity for elevated neuroinflammatory cytokine production. Using the well-established 5 xFAD model of AD to interrogate neuroinflammatory regulation, impairment of LANDO through deletion of a key upstream regulator Rubicon or other downstream autophagy components, exacerbated disease onset and severity, while deletion of microglial autophagy alone had no measurable effect. Mice presented with robust deposition of the neurotoxic AD protein β-amyloid(Aβ), microglial activation and inflammatory cytokine production, tau phosphorylation, and aggressive neurodegeneration culminating in severe memory impairment. LANDO-deficiency impaired recycling of receptors that recognize Aβ, including TLR4 and TREM2. LANDO-deficiency alone through deletion of the WD-domain of the autophagy protein ATG16 L, revealed a role for LANDO in the spontaneous establishment of age-associated AD. LANDO-deficient mice aged to 2 years presented with advanced ADlike disease and pathology correlative to that observed in human AD patients. Together, these studies illustrate an important role for microglial LANDO in regulating CNS immune activation and protection against neurodegeneration. New evidence is emerging that demonstrates a putative linkage between pathways such as LANDO and cell death regulation via apoptosis and possibly necroptosis. Herein, we provide a

关键词： aging Alzheimer's disease autophagy inflammation LC3-associated endocytosis microglia neurodegeneration neuroinflammation