http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Mackey, David (검색결과 15 건)
- 무료
- 기관 내 무료
- 유료
-
Proteasome-Dependent Degradation of RPM1 Desensitizes the RPM1-Mediated Hypersensitive Response
Mackey David,윤대진,Nam Jaesung 한국식물학회 2021 Journal of Plant Biology Vol.64 No.3
The intracellular plant resistance (R) proteins, nucleotide-binding and leucine-rich repeat (NLR) proteins, mediate resistance to pathogens by enabling recognition and rapid response. The response consists of the induction of a defensive suite that typically culminates in the hypersensitive response (HR), death of the plant cells at and around an infection site. The Arabidopsis intracellular innate immune receptor protein RESISTANCE TO PSEUDOMONAS MACULICOLA1 (RPM1) is a coiled-coil (CC) type of NLR protein that specifies resistance to strains of the bacterial pathogen Pseudomonas syringae expressing the type III effector proteins AvrRpm1 and AvrB. We previously demonstrated that RPM1-myc (an epitope-tagged version of RPM1) disappears coincident with the onset of HR induced by AvrRpm1. Infection with P. syringae expressing two other type III effector proteins, AvrRpt2 and AvrRps4, also initiated RPM1-myc disappearance at time points coincident with the HR they initiate through the NLR proteins RESISTANCE TO P. SYRINGAE2 (RPS2) and RESISTANCE TO P. SYRINGAE 4 (RPS4), respectively. Here, we use mutants impaired in NLR gene dependent signaling to demonstrate that disappearance of RPM1-myc requires normal NLR gene dependent signaling steps, but does not require HR. Inhibitors of the 26S proteasome block the disappearance of RPM1-myc and enhance RPM1-myc-dependent cell death. Our data are consistent with a model in which RPM1 is degraded by the 26S proteasome to limit the extent of RPM1-dependent signaling and/or cell death. Furthermore, AvrRpt2 induces disappearance of RPM1-myc in rps2 mutant plants without HR, suggesting that RPM1 is part of the host target of the virulence activity of AvrRpt2.
-
Michael Mackey,Laurena Holleran,Gary Donohoe,Declan P. McKernan 대한신경정신의학회 2022 PSYCHIATRY INVESTIGATION Vol.19 No.12
Objective Immune system dysregulation is hypothesised to be central to the aetiopathogenesis of schizophrenia; however, the role of sterile inflammation remains unclear. Damage associated molecular patterns are key initiators of sterile inflammation and are detectable in peripheral blood. Methods A defined systematic search of the Web of Science, PubMed, and Scopus was performed to identify adult case-control studies published between January 1990 and June 2022. Three studies consisting of 242 cases and 83 controls met inclusion for the systematic review and meta-analysis of HMGB1 while twenty-eight studies consisting of 1,544 cases and 1,248 healthy controls were included for S100B. Results A significant standardised mean difference in peripheral S100B and HMGB1 concentrations was detected between cases and controls. S100B subgroup analysis determined the largest significant effect size for unmedicated individuals diagnosed with schizophrenia. Conclusion This study provides evidence that peripheral S100B and HMGB1 concentrations are elevated in individuals diagnosed with schizophrenia when compared with healthy controls. These results should be interpreted with caution as significant heterogeneity was present during meta-analysis of S100B in the entire sample and in sub-group analysis. The persistence of significant heterogeneity throughout subgroup analysis indicates that the current diagnostic groupings may be a barrier to understanding human behaviours and emotions.
-
-
Adsorbent minimisation in a two-stage batch adsorber for cadmium removal
Haya Alyasi,Hamish R. Mackey,Kavithaa Loganathan,Gordon McKay 한국공업화학회 2020 Journal of Industrial and Engineering Chemistry Vol.81 No.-
Cadmium is a toxic metal prevalent in a variety of industrial effluents that is toxic to both humans andanimals. This study utilizes nanochitosan, a polymer derived from crustacean shells, as an adsorbent forcadmium removal. The uptake capacity has been determined at 2.01 mmol/g and modelled by Langmuir,Freundlich and Sips isotherms, with the Sips isotherm the most suitable model for the adsorbent. In orderto minimise the amount of adsorbent used in a batch treatment process for the cadmium removal, a two-stage batch treatment has been proposed and optimised. A detailed evaluation is made of theconsequences of utilizing a less suitable isotherm, and on the benefits of utilizing a two-stage system overa single stage. Both errors from incorrect isotherms and advantages of a two-stage system are mostsignificant at low influent concentrations and high target removal efficiencies, relevant to environmentalregulatory discharge limits.
-
-
Geng, Xueqing,Shen, Mingzhe,Kim, Jin Hee,Mackey, David Springer-Verlag 2016 Plant cell reports Vol.35 No.4
<P>Type III effectors AvrRpm1 and AvrRpt2 promote bacterial growth dependent on a COI1-mediated pathway in the absence of the RPM1 and RPS2 resistance proteins. The type III effectors, AvrRpm1 and AvrRpt2, promote bacterial virulence by suppressing host defense responses. The defense suppressing activities of AvrRpm1 and AvrRpt2 are best studied in the absence of the resistance proteins RPM1 and RPS2, which induce defense responses to them. We tested whether the type III effectors could modulate a CORONATINE INSENSITIVE1 (COI1)-mediated hormone signaling pathway to promote virulence. COI1 has been demonstrated to contribute in the induction of chlorosis during Pseudomonas syringae infection. By comparing the activity of inducibly expressed AvrRpm1-HA or AvrRpt2-HA in rpm1rps2 and rpm1rps2coi1 backgrounds, we demonstrate that both effectors promote bacterial growth dependent on a COI1-mediated pathway and additively with the action of coronatine (COR) and that AvrRpt2-HA induces COI1-dependent chlorosis. Further, PATHOGENESIS RELATED1 (PR-1) expression resulting from inducible expression of AvrRpm1-HA or AvrRpt2-HA is elevated in coi1 plants consistent with the effectors activating JA-signaling to antagonize SA-signaling. In addition, we found that AvrRpm1-HA or AvrRpt2-HA requires COI1 to promote bacterial growth through suppression of both SA-dependent and SA-independent defense responses. Collectively, these results indicate that type III effectors AvrRpm1 and AvrRpt2 promote bacterial virulence by targeting a COI1-dependent signaling pathway.</P>
-
Responses of Arabidopsis thaliana to Challenge by Pseudomonas syringae
Kim, Min Gab,Kim, Sun Yong,Kim, Woe Yeon,Mackey, David,Lee, Sang Yeol Korean Society for Molecular Biology 2008 Molecules and cells Vol.25 No.3
Plants are continually exposed to a variety of potentially pathogenic microbes, and the interactions between plants and pathogenic invaders determine the outcome, disease or disease resistance. To defend themselves, plants have developed a sophisticated immune system. Unlike animals, however, they do not have specialized immune cells and, thus all plant cells appear to have the innate ability to recognize pathogens and turn on an appropriate defense response. Using genetic, genomic and biochemical methods, tremendous advances have been made in understanding how plants recognize pathogens and mount effective defenses. The primary immune response is induced by microbe-associated molecular patterns (MAMPs). MAMP receptors recognize the presence of probable pathogens and evoke defense. In the co-evolution of plant-microbe interactions, pathogens gained the ability to make and deliver effector proteins to suppress MAMP-induced defense responses. In response to effector proteins, plants acquired R-proteins to directly or indirectly monitor the presence of effector proteins and activate an effective defense response. In this review we will describe and discuss the plant immune responses induced by two types of elicitors, PAMPs and effector proteins.
-
Kim, Min Gab,Geng, Xueqing,Lee, Sang Yeol,Mackey, David Blackwell Publishing Ltd 2009 The Plant journal Vol.57 No.4
<P>Summary</P><P>Plant disease resistance (R) proteins recognize potential pathogens expressing corresponding avirulence (Avr) proteins through ‘gene-for-gene’ interactions. RPM1 is an Arabidopsis R-protein that triggers a robust defense response upon recognizing the <I>Pseudomonas syringae</I> effector AvrRpm1. Avr-proteins of phytopathogenic bacteria include type III effector proteins that are often capable of enhancing virulence when not recognized by an R-protein. In <I>rpm1</I> plants, AvrRpm1 suppresses basal defenses induced by microbe-associated molecular patterns. Here, we show that expression of AvrRpm1 in <I>rpm1</I> plants induced PR-1, a classical defense marker, and symptoms including chlorosis and necrosis. PR-1 expression and symptoms were reduced in plants with mutations in defense signaling genes (<I>pad4</I>, <I>sid2</I>, <I>npr1</I>, <I>rar1</I>, and <I>ndr1</I>) and were strongly reduced in <I>rpm1 rps2</I> plants, indicating that AvrRpm1 elicits defense signaling through the Arabidopsis R-protein, RPS2. Bacteria expressing AvrRpm1 grew more on <I>rpm1 rps2</I> than on <I>rpm1</I> plants. Thus, independent of its classical ‘gene-for-gene’ activation of RPM1, AvrRpm1 also induces functionally relevant defenses that are dependent on RPS2. Finally, AvrRpm1 suppressed host defenses and promoted the growth of type III secretion mutant bacteria equally well in <I>rps2</I> and <I>RPS2</I> plants, indicating that virulence activity of over-expressed AvrRpm1 predominates over defenses induced by weak activation of RPS2.</P>
-
-
Geng, Xueqing,Jin, Lin,Shimada, Mikiko,Kim, Min Gab,Mackey, David Springer Berlin Heidelberg 2014 Planta Vol.240 No.6
<P>Plant pathogens deploy an array of virulence factors to suppress host defense and promote pathogenicity. Numerous strains of <I>Pseudomonas syringae</I> produce the phytotoxin coronatine (COR). A major aspect of COR function is its ability to mimic a bioactive jasmonic acid (JA) conjugate and thus target the JA-receptor COR-insensitive 1 (COI1). Biological activities of COR include stimulation of JA-signaling and consequent suppression of SA-dependent defense through antagonistic crosstalk, antagonism of stomatal closure to allow bacterial entry into the interior of plant leaves, contribution to chlorotic symptoms in infected plants, and suppression of plant cell wall defense through perturbation of secondary metabolism. Here, we review the virulence function of COR, including updates on these established activities as well as more recent findings revealing COI1-independent activity of COR and shedding light on cooperative or redundant defense suppression between COR and type III effector proteins.</P>
KCI
스콜라연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
