Relevant Degree Programs
Systemic acquired resistance, SA signaling, ROS signaling, MAPK signaling, signal transduction pathways downstream of plant immune receptors
Complete these steps before you reach out to a faculty member!
- Familiarize yourself with program requirements. You want to learn as much as possible from the information available to you before you reach out to a faculty member. Be sure to visit the graduate degree program listing and program-specific websites.
- Check whether the program requires you to seek commitment from a supervisor prior to submitting an application. For some programs this is an essential step while others match successful applicants with faculty members within the first year of study. This is either indicated in the program profile under "Admission Information & Requirements" - "Prepare Application" - "Supervision" or on the program website.
- Identify specific faculty members who are conducting research in your specific area of interest.
- Establish that your research interests align with the faculty member’s research interests.
- Read up on the faculty members in the program and the research being conducted in the department.
- Familiarize yourself with their work, read their recent publications and past theses/dissertations that they supervised. Be certain that their research is indeed what you are hoping to study.
- Compose an error-free and grammatically correct email addressed to your specifically targeted faculty member, and remember to use their correct titles.
- Do not send non-specific, mass emails to everyone in the department hoping for a match.
- Address the faculty members by name. Your contact should be genuine rather than generic.
- Include a brief outline of your academic background, why you are interested in working with the faculty member, and what experience you could bring to the department. The supervision enquiry form guides you with targeted questions. Ensure to craft compelling answers to these questions.
- Highlight your achievements and why you are a top student. Faculty members receive dozens of requests from prospective students and you may have less than 30 seconds to pique someone’s interest.
- Demonstrate that you are familiar with their research:
- Convey the specific ways you are a good fit for the program.
- Convey the specific ways the program/lab/faculty member is a good fit for the research you are interested in/already conducting.
- Be enthusiastic, but don’t overdo it.
G+PS regularly provides virtual sessions that focus on admission requirements and procedures and tips how to improve your application.
Graduate Student Supervision
Doctoral Student Supervision (Jan 2008 - Nov 2019)
No abstract available.
Activated plant defense responses consist of PAMP (pathogen associated molecular pattern)-triggered immunity (PTI) and effector-triggered immunity (ETI) at infected sites and a secondary immune response in distal parts of the host plant, termed systemic acquired resistance (SAR). Salicylic acid (SA) plays critical roles in plant immunity and its level increases upon pathogen infection. Pathogen-induced SA biosynthesis predominantly relies on ICS1 (ISOCHORISMATE SYNTHASE 1), whose induction mainly depends on transcription factors SARD1 (SAR DEFICIENT 1) and CBP60g (CALMODULIN BINDING PROTEIN 60 g). Meanwhile, the expression of SARD1 and CBP60g is also highly induced by pathogens. My Ph.D. research focuses on identification of immune regulators that function upstream and downstream of SARD1 and CBP60g. First, we performed chromatin immunoprecipitation-sequencing experiments to identify candidate targets of SARD1. We found that SARD1 and CBP60g directly control the expression of a large number of key regulators involved in PTI, ETI and SAR. Among them, two genes essential for SAR, ALD1 (AGD2-LIKE DEFENSE RESPONSE PROTEIN 1) and SARD4, are involved in the biosynthesis of pipecolic acid (Pip), a plant secondary metabolite required for SAR. Consistently, the sard1cbp60g double mutant accumulates less Pip than wild type, suggesting that SARD1 and CBP60g regulate Pip biosynthesis in addition to SA. Secondly, we showed that transcription factors TGA1 and TGA4 act upstream of SARD1 and CBP60g and thus regulate the biosynthesis of SA and Pip. Lastly, we revealed a novel mechanism of SA perception by its receptors NPR3 (NPR1-LIKE PROTEIN 3) and NPR4. NPR3/NPR4 interact with transcription factors TGA2, TGA5 and TGA6, and act as transcriptional repressors. SA inhibits the transcriptional repression activities of NPR3/NPR4 and promotes the transcriptional activation activity of NPR1 (NONEXPRESSER OF PR GENES 1); both contribute to SA-induced defense gene expression. We also found that SA induces SARD1 expression, revealing a feedback amplification loop between SA and SARD1, where SARD1 promotes SA biosynthesis via directly activating ICS1 expression and SA induces SARD1 expression by regulating the activities of NPR/TGA complexes. Altogether studies in this dissertation provide new insights on the functions of SARD1 and CBP60g in plant immunity and the mechanism of SA perception and signaling.
Plant immunity is usually governed by two types of immune receptors: 1) pattern recognition receptors (PRRs) recognize the conserved molecular features of pathogens (pathogen-associated molecular patterns, PAMPs) and trigger PTI (PAMP-triggered immunity) and 2) nucleotide-binding and leucine-rich repeats-containing proteins (NLRs) serve as intracellular immune receptors to recognize the presence of relatively diverse pathogen effectors and trigger ETI (effector-triggered immunity). The Arabidopsis thaliana mutant snc2-1D (suppressor of npr1-1, constitutive 2) contains a gain-of-function mutation in a receptor-like protein (RLP) and displays a dwarf morphology. Here I report the characterization of bda4-1D (bian da 4-1D), which was identified as a complete suppressor of snc2-1D dwarf morphology. Positional cloning showed bda4-1D contains a gain-of-function mutation in Non-Expressor of Pathogenesis-Related Proteins 4 (renamed npr4-4D). Functional analysis indicated NPR4, as well as its close homolog NPR3 (Non-Expressor of Pathogenesis-Related Proteins 3), function as transcriptional repressors. They function downstream of SNC2, independent of NPR1 (Non-Expressor of Pathogenesis-Related Proteins 1). In addition, salicylic acid (SA) was shown to inhibit the transcriptional activities of NPR3/4 and promote the expression of key immune regulators. The npr4-4D mutation leads to constitutive repression of SA-induced immune responses, indicating that the mutant protein can no longer respond to SA. On the other hand, the equivalent mutation in NPR1 also abolishes its ability to bind SA and renders reduced SA-induced defence gene expression. My results demonstrated that both NPR1 and NPR3/NPR4 are bona fide SA receptors, but play opposite roles in transcriptional regulation of SA-induced defence gene expression.In the independent eds5-3 snc2-1D npr1-1 suppressor screen, I report the identification and characterization of four more bda mutants, bda3-1D, bda5-1, bda6 and bda7. Cloning of BDA6 and BDA7 showed that they encode FMO1 and ALD1 respectively, which are involved in biosynthesis of N-Hydroxypipecolic Acid (NHP) and pipecolic acid. My results indicate that enzymes involved in Lysine metabolism are also important for signaling in SNC2-mediated immune pathway.Overall, the studies I completed in my Ph.D. thesis expand our knowledge in understanding of the signaling pathways downstream of SNC2 as well as the general regulatory mechanisms of SA receptors in plant innate immunity.
The diamondback moth (DBM), Plutella xylostella, is well known for its extensive adaptation and distribution, high level of genetic variation and polymorphism, and strong resistance to a broad range of synthetic insecticides. Although understanding of the P. xylostella biology and ecology has been considerably improved, knowledge on the genetic basis of these traits remains surprisingly limited. Based on data generated by different sets of molecular markers, we uncovered the history of evolutionary origin and regional dispersal, identified the patterns of genetic diversity and variation, characterized the demographic history, and revealed natural and human-aided factors that are potentially responsible for contemporary distribution of P. xylostella. These findings rewrite our understanding of this exceptional system, revealing that South America might be a potential origin of P. xylostella, and recently colonized across most parts of the world resulting possibly from intensified human activities. With the data from selected continents, we demonstrated signatures of localized selection associated with environmental adaptation and insecticide resistance of P. xylostella. This work brings us to a better understanding of the regional movement and genetic bases on rapid adaptation and development of agrochemical resistance, and provides a solid foundation for better monitoring and management of this worldwide herbivore and forecast of regional pest status of P. xylostella, by taking a cost-effective response to insecticide resistance and better implementation of biological control programs.
Master's Student Supervision (2010 - 2018)
As an early defense response, MAP kinase cascade activation plays important roles in transduction and amplification of signals upon pathogen perception in plants. The Arabidopsis MEKK1-MKK1/MKK2-MPK4 kinase cascade was previously shown to negatively regulate plant immunity. In this study, two suppressors of the mkk1 mkk2 double mutant – summ4-1D and summ4-2D have been identified and characterized. summ4-1D and summ4-2D contain mutations in the promoter region of MKK6, which leads to elevated expression of MKK6, causing suppression of the mkk1 mkk2 autoimmune phenotypes. However, the autoimmune phenotypes of mekk1 and mpk4 cannot be suppressed by summ4-1D. MKK6 interacts with MEKK1 and MPK4, and MPK4 activation is blocked in mkk1 mkk2, but is recovered in the summ4-1D mkk1 mkk2 triple mutant background. These results suggest that MKK6 functions in parallel with MKK1 and MKK2 to negatively regulate plant immunity.
Recognition of pathogens through pathogen-associated molecular patterns (PAMPs) or effectors in plants activates a variety of defense responses including MAPKs signaling pathways and defense related genes expression. ANPs (Arabidopsis Nucleus- and Phragmoplast- localized kinase 1 related protein kinases), including ANP1, ANP2, ANP3 are three MAP kinase kinase kinases that form a MAP kinase cascade with downstream MKK6 and MPK4 to regulate cytokinesis process. In this study, we showed that the anp2 anp3 double mutants exhibit constitutive expression of PR (Pathogenesis-Related) genes and enhanced resistance against oomycete pathogen H. a. Noco2, suggesting that ANP2 and ANP3 negatively regulate plant immunity. In addition, loss function of MKK6 causes high levels of PR gene expression, indicating that MKK6 is involved in negative regulation of defense responses. Since MPK4 was previously shown to function as a negative regulator of plant immunity, we tested whether MPK4 functions downstream of ANP2/ANP3 and MKK6 in plant immunity by introducing CA-MPK4 transgene, which expresses a constitutively active (CA) variant of MPK4, to anp2 anp3 and mkk6. Constitutive expression of PR genes and enhanced resistance to H.a. Noco2 in anp2 anp3 and mkk6 were partially suppressed by expressing CA MPK4, suggesting that the ANP2/ANP3, MKK6 and MPK4 function in a MAPK cascade to negatively regulate defense responses. To find out components that function downstream of ANP2/ANP3- MKK6-MPK4 cascade in plant immunity, two mutants summ2-8 (SUPPRESSOR OF MKK1 MKK2 2) and pad4-1 (PHYTOALEXIN DEFICIENT 4) were crossed into anp2 anp3 respectively. The constitutive defense responses in anp2 anp3 were fully suppressed by pad4-1, but not affected by the summ2-8 mutation, suggesting that PAD4 functions downstream of ANP2/ANP3 and that immune responses mediated by certain TIR-NB-LRR R proteins might be activated in the anp2 anp3 mutant.
Plants are sessile organisms that are surrounded by pathogens. To stay healthy, they need a complex and sensitive immune system. Specific pattern-recognition receptors (PRRs) localized on the plasma membrane can recognize conserved motifs from pathogens and transduce the signal into the cell to initiate defence responses. The receptor-like kinase BAK1-INTERACTING RECEPTOR-LIKE KINASE 1 (BIR1), functions as a negative regulator of plant immunity. bir1-1 exhibits spontaneous cell death and constitutive defence responses that are dependent on SUPPRESSOR OF BIR1,1 (SOBIR1) and PHYTOALEXIN DEFICIENT 4 (PAD4). Here I present the evidence that ER-quality control, a collective mechanism ensuring that only native proteins are produced by the secretary pathway, plays important roles in regulating defence responses in bir1-1. Five components in ER-quality control pathways, including CRT3, UGGT, STT3a, ERdj3b and SDF2, are all required for the immune responses in bir1-1. Western blot analysis showed that mutations in CRT3, ERdj3b and UGGT lead to reduced accumulation of SOBIR1 protein. The data suggest that ER-quality control plays an important role in the accumulation of SOBIR1 and is required for the defence responses in bir1-1.