Tandem Protein Kinases Emerge as New Regulators of Plant Immunity
Name: Valentyna Klymiuk
Current Position: Postdoctoral researcher, Crop Development Centre and Department of Plant Sciences, University of Saskatchewan, Saskatoon, Canada.
Education: M.S. and Ph.D. degrees in hydrobiology at Donetsk National University, Donetsk, Ukraine; Ph.D. degree in plant genomics and host-parasite interactions at the University of Haifa, Haifa, Israel.
Non-scientific Interest: Hiking, playing piano, cross-stitching.
Brief Bio: I obtained my B.S., M.S., and one of two Ph.D. degrees from Donetsk National University, Ukraine. These degrees were in the area of hydrobiology, in which I focused on biodiversity and ecology of microalgae communities of continental salt lakes. Because of my growing interest in genetics and genomics, I decided to continue my studies, and I completed a second Ph.D. degree from the University of Haifa, Israel, where my studies focused on plant genomics and host-parasite interactions. Currently, I am a postdoctoral research fellow studying the genetic basis of disease resistance in wheat and its wild relatives. More specifically, I have studied innate resistance to wheat diseases, with an emphasis on identification, gene cloning, and functional characterization of tandem kinase proteins (TKP). Decades of research on canonical immune receptors, exhibiting nucleotide-binding leucine-rich repeat (NBS-LRR) or receptor-like protein (RLP)/receptor-like kinase (RLK) architectures, have firmed their established role in plant immune response. However, there is a general lack of focus on other receptor types, such as TKPs, and my interest lies in shedding light on the role of this important protein family in plant immune response. Currently, one barley and four wheat TKP genes have been functionally validated, but many more have yet to be discovered because TKPs are widespread and diverse across the plant kingdom. To bring more attention to TKPs and highlight their role in plant immunity, together with other co-authors from this research field, I published a review article in MPMI that provides the first comprehensive summary of information for all functionally validated TKPs. A detailed literature review also allowed us to propose a model of TKP evolution through duplication or fusion event and model of molecular function, in which the pseudokinase domain is suggested to serve as a decoy for pathogen effector, while the kinase domain is essential for downstream signaling. I believe that this work provides a deeper investigation of TKPs and will pave the way for future gene manipulation and synthetic engineering of novel plant resistance genes.
The December 2020 Editor’s Pick
for MPMI is “Sec-Delivered
Effector 1 (SDE1) of ‘Candidatus
Liberibacter asiaticus’ Promotes Citrus Huanglongbing,”
in which Kelley Clark
and co-authors demonstrate the effect that the SDE1 protein from the citrus greening
(huanglongbing) pathogen can have on plants. Their results show that the effector
is an important virulence factor that induces premature senescence-like responses
in both Arabidopsis and citrus host plants.
Sec-Delivered Effector 1 (SDE1)
Liberibacter asiaticus’ Promotes Citrus Huanglongbing
Name: Kelley J. Clark
Postdoctoral researcher, University of Arkansas (located at USDA-ARS Salinas, CA).
Ph.D. degree in microbiology and plant pathology at the University of California,
Riverside, and B.S. degree in plant sciences at the University of Arizona.
Gardening, traveling to national parks, hiking, walking my cat.
Bio: Currently, I am a postdoctoral researcher for the University
of Arkansas, but stationed in Salinas, CA, at the USDA-ARS facilities. My research
project is on spinach downy mildew, and I am located in the Salinas Valley because
it is the “salad bowl of the world,” producing the majority of the leafy greens
we consume! The research recently published in MPMI is the final chapter of my Ph.D. thesis from
my time at UC Riverside under the supervision of Prof. Wenbo Ma. Our overarching goal was
to understand how an effector of Candidatus Liberibacter asiaticus contributes to huanglongbing
(HLB) disease progression. More specifically, for this publication we wanted to
understand how the effector SDE1 contributes to leaf yellowing in Arabidopsis and
how this relates to HLB yellowing symptoms in citrus.
project challenged me on many levels, both intellectually and emotionally, especially
as my passion for research progressed and I grew as a scientist. The HLB-associated
pathogen, Ca. L.
asiaticus, is obligate, which presents many obstacles, but also opportunities, for
novel research. During my Ph.D. studies, I was fortunate to learn several new techniques,
have access to state-of-the art technology, and collaborate with distinguished scientists.
For this project, we had access to SDE1-transgenic citrus, which would not have
been possible without help from our collaborators Prof. Nian Wang and Dr. Zhiqian Pang at the
University of Florida. Additionally, we implemented NanoString technology to directly
measure the transcript quantity of specific genes in citrus. Although this technology
is widely used in medical research, it holds tremendous potential for plant–microbe
interaction research, as well as other fields of study.
addition to gaining a technical skill set, I grew passionate about citriculture
from studying its history in Riverside, CA. When I moved to Riverside to pursue
my Ph.D. research, I volunteered at the California Citrus State Historic Park. The
park consists of more than 250 acres of citrus groves showcasing more than 80 different
citrus varieties and includes a museum highlighting the history of citrus in California.
Did you know that Riverside is home to the parent Navel orange tree planted by Eliza Tibbets
tree is still alive today,
and you can visit it on the corner of Magnolia and Arlington Streets, but due to
the threat of HLB, the tree is covered with a mesh tent to keep out the insect vector
that transmits Ca.
L. asiaticus. Volunteering at the park gave me the opportunity to immerse myself
in the rich culture of citrus and see others admire it is as well, which drove my
research efforts, since HLB continues to threaten not only the citrus industry,
but our connection to its past, present, and future.
look forward to working on more challenging and insightful projects in the future,
incorporating both the knowledge I gained from this research and the inspiration
I drew from learning about the agricultural history of a specific crops.
The May 2020 Editor’s pick for MPMI
Response Regulator 6 (ARR6) Modulates Plant Cell-Wall Composition and Disease
The first author is Laura Bacete, a graduate student in the lab of Antonio Molina at the Universidad
Politécnica de Madrid. To read
more about Laura, you can find her bio here.
Laura is now a postdoc at the Institute for Biology at the Norwegian University
of Science and Technology. Antonio recently presented this work in a What’s
New in MPMI? Seminar. You can find a recording of his seminar here.
Plant Cell Wall Composition and Disease Resistance:
A Journey across Novel Mechanisms of Plant Immunity
Submitted by Laura Bacete and Antonio
Traditionally, the plant cell wall has been
considered simply a physical defensive barrier against pathogens. However, this
outdated view has evolved to a novel concept that considers the plant cell wall
as a dynamic structure regulating different processes of plant immunity and development
(Figure 1) (Bacete et al. 2018). Recently, we have published
in Molecular Plant-Microbe Interactions (MPMI) our last findings about
the impact of the alteration of the cytokinin-responsive Arabidopsis Response
Regulator 6 (ARR6) gene expression
on the modulation of plant cell wall composition and disease resistance responses
(Bacete et al. 2020). Here, we describe the
story of how we reached this fascinating discovery, and how our research group,
initially focused on A. thaliana resistance
to necrotrophic fungi, started a journey that led us to identify a novel mechanism
of plant immunity and to determine the relevance of plant cell wall composition
in disease resistance. This journey led us to the conviction that plant cell wall-mediated
immunity is a key and dynamic component of plant disease resistance against necrotrophic
fungi—our initial pathogens of interest—but also against all the plant pathogens
we have studied.
The complexity of the plant immune system
The complexity of the plant immunity
system, comprising different mechanisms of resistance, was well known at the beginning
of this century. These mechanisms include diverse molecular monitoring systems that
perceive stresses-derived signals, as well as microbe-associated molecular patterns
(MAMPs) and effectors (avirulent proteins) from pathogens, which trigger specific
resistance responses upon perception by specific plant receptors (Jones and Dangl 2006). The evolution of such
monitoring systems has enabled plants to fine-tune their defensive responses
and to adapt their physiological response to environmental condition changes. Also,
it is well known that plant defensive responses are mediated by phytohormones, like
salicylic acid (SA), ethylene (ET), and jasmonic acid (JA), which were initially
described as mainly required for plant resistance to biotrophic (SA) and nectrotrophic
(ET and JA) pathogens, respectively (Robert-Seilaniantz
et al. 2011). In recent years, other phytohormones have been added to
this list of “defensive hormones.” These include abscisic acid (ABA),
brassinosteroids, gibberellins, auxins, and more recently cytokinin, as shown in
recent articles and in our MPMI paper (Bacete
et al. 2020; Argueso et al. 2012; Gupta et al. 2020).
Two decades ago, the plant cell wall was considered
in the plant immunity field to be simply a structure displaying a physical defensive
role—a sort of passive barrier with no essential function in a complex plant
immune system. Nevertheless, it had been demonstrated by several groups that the
plant cell wall is a dynamic and highly regulated structure with several
important functions for plant growth and development. All plant cells have a primary
plant cell wall that is mainly composed of cellulose—which is the principal load-bearing
component—pectins, hemicelluloses, and structural
glycoproteins. In addition, cells that have completed their cellular expansion and
need to strengthen their structure for functional reasons (e.g., to form vessel
or fiber cells) generate a secondary cell wall that also includes lignin.
The plant cell wall is a prominent structure to manage mechanical stresses
caused by either internal (e.g., due to osmotic pressure) or external (e.g.,
caused by pathogen attack) physiological/environmental changes. Therefore, an
important question arose several years ago: how do plants perceive these
changes in their cell walls? In recent years, the status of the plant cell wall
has been shown to be constantly monitored through a series of cell wall integrity
(CWI) surveillance mechanisms (Bacete and Hamann
2020), and the wall has been found to be a source of damage-associated molecular
patterns (DAMPs), mainly of carbohydrate-based compositions, that trigger immune
responses (Bacete et al. 2018, 2020).
thaliana disease resistance to necrotrophic fungi: The initials
Early in the foundation
of our lab at the Technical University of Madrid (UPM, Spain), we performed several
screenings of A. thaliana mutant collections and quantitative trait loci
(QTL) analyses of ecotypes to identify novel genetic components of plant resistance
to necrotrophic fungi. The reason for this initial objective was that the genetic
determinants of plant resistance to this type of fungi were understudied,
despite the fact that necrotrophic fungi cause important yield loses in
agriculture. We selected for these initial screenings several strains from different
necrotrophic fungi species, but we particularly focused on one strain that had been
serendipitously isolated by Brigitte Mauch-Mani (Neuchatel University,
Switzerland) from Arabidopsis plants growing under her lab conditions (Ton and Mauch-Mani 2004). This necrotrophic fungal strain
was an ascomycete from Plectosphaerella cucumerina, which was very easy to
handle in the lab and, more importantly, gave very reproducible necrotrophic symptoms
in different A. thaliana genotypes. We named this isolate PcBMM to
recognize the contribution of Brigitte Mauch-Mani to its discovery. PcBMM
transformed our scientific goals, changed our view of the genetic determinants of
plants resistance to necrotrophic fungi, and revealed an unexpected and relevant
contribution of the plant cell wall to immunity. This exciting journey with Plectospherella
has recently reached an important milestone with the publication in MPMI
of the first sequence and annotation of the genomes and transcriptomes of three
Plectospherella strains (including PcBMM) with different lifestyles
on A. thaliana genotypes (Muñoz-Barrios
et al. 2020).
In our early screenings
with PcBMM we identified several A. thaliana cell wall mutants, like
ern1/irx1/lew2 (impaired in AtCESA8 required for secondary cell wall
cellulose synthesis), displaying broad-spectrum resistance to PcBMM and other
necrotrophic and biotrophic pathogens and enhanced resistance to abiotic
stresses. This initial finding was shocking, but exciting, since it was not in accordance
with the classical view of plant disease resistance to necrotrophic pathogens. Intriguingly,
the molecular bases of irx1 resistance did not seem to be dependent on canonical
defensive pathways (e.g., the expected ET and JA for necrotrophic fungi), but instead
it relied on novel mechanisms of immunity involving ABA signaling and antimicrobial
compounds like tryptophan-derived metabolites and peptides (Hernandez-Blanco et al. 2007). Moreover, in additional
screening aimed at deciphering PcBMM genetic resistance, we frequently found
A. thaliana mutants with enhanced susceptibility to PcBMM and additional
pathogens, which showed alterations in their plant cell wall composition. Among
these mutants were erecta (er), impaired in a receptor-like protein
kinase, and agb1, defective in the beta-subunit of Arabidopsis heterotrimeric
G protein, that display different biochemical alterations in their cell wall composition
compared with that of wild-type plants (Delgado-Cerezo
et al. 2012; Llorente et al., 2005; Sánchez-Rodríguez et al. 2009; Torres et al. 2013). These and additional exciting results suggested that ER and heterotrimeric
G proteins play roles in regulating novel mechanisms of disease resistance mediated
by the cell wall in addition to their function in plant development (Sánchez-Rodríguez
et al. 2009). The function of ER-mediated
pathway in immunity was further corroborated by the characterization of the role
in plant immunity of YODA, a mitogen-activated protein kinase kinase kinase (MAPK3)
functioning downstream of ER in plant development (Bergmann 2004). YODA has been found to regulate broad-spectrum disease resistance through
noncanonical defensive mechanisms involving cell wall-mediated resistance and the
up-regulation of the expression of specific protein receptors and peptidic DAMPs
(Sopeña-Torres et al. 2018; Téllez et al. 2020).
contribution of the plant cell wall to A. thaliana immunity: The ARR6
The findings described
above led us to the conviction that plant cell wall composition and integrity were
essential components of A. thaliana
immunity. To explore this regulatory
effect of the plant cell wall on A. thaliana
immunity and resistance to different
type of pathogens, we decided to follow a biased mutant screening approach and to
perform a detailed analysis of the resistance to different pathogens of a collection
of selected Arabidopsis
mutants impaired in either the primary or secondary
cell wall (Molina et al. 2020). In this biased
screening (Figure 2
an astonishingly high number of cell wall mutants showed altered susceptibility/resistance
to one or more of the pathogens tested compared with wild-type plants, further supporting
the key contribution of the plant cell wall to disease resistance (for further details are provided in Molina et al. 2020).
One of the cell wall
mutants with disease resistance alterations was impaired in the ARR6 gene (arr6), and it is
characterized in our MPMI paper (Bacete et al. 2020). Our first observations
on two mutant alleles (arr6-3 and arr6-2) of ARR6 indicated
that they both had alterations in their cell wall composition and in their resistance
to different pathogens with different colonization styles. ARR proteins have been
described as components of the cytokinin signaling pathway, which has previously
been involved in the modulation of some disease-resistance responses (Argueso et al. 2012; Gupta et al. 2020). In
our work recently published in MPMI (Bacete
et al. 2020), we describe a previously unknown function of ARR6 by
showing that ARR6 is actually a regulator of cell wall composition and of disease
resistance responses against different pathogens causing important diseases,
like the necrotrophic fungus PcBMM and the vascular bacterium Ralstonia
solanacearum. arr6 mutants, which do not have functional versions of the ARR6
gene, are more resistant to PcBMM fungus but more rapidly and intensely develop
the disease symptoms caused by the vascular bacterium R. solanacearum. In
contrast, plants that display higher levels of ARR6 expression (by
transgenic overexpression) than wild-type plants or arr6-3 (e.g.,
overexpressor and complementation lines, respectively) are more resistant to the
bacteria but more susceptible to the fungus. Transcriptomic and metabolomic analyses
revealed that, in arr6 plants, canonical
disease-resistance pathways, like those activated by defensive phytohormones, were
not altered, whereas immune responses triggered by microbe-associated molecular
patterns were slightly enhanced. As in previous research approaches performed
in the lab, our findings of the bases of the resistance were again original and
out of the canons, which is something that always triggers researchers’
curiosity, making our work even more intriguing and exciting, but also risky
for publication. Moreover, the characterization of ARR6-mediated resistance reinforced
our view of plant cell wall relevance in the modulation of specific immune responses
and confirmed the opportunities provided by plant cell wall mutants for the identification
of novel and uncharacterized mechanisms of plant immunity.
hypothesized that some cell wall component could be released from arr6 walls due to their observed alteration in composition and that
this compound might function as DAMP that will be recognized by a plant
receptor, triggering immunity. However, cell walls are very complex, so we had
to obtain simpler cell wall fractions enriched in main biochemical components. Remarkably,
pectin-enriched cell wall fractions from arr6 plants activated more intense
immune responses than similar wall fractions from wild-type plants, suggesting that
the arr6 pectin fraction is enriched in wall-related DAMPs. The next step
we performed in this research area was the purification of these putative DAMP molecules
from arr6 pectin fractions. Actually, we have recently described the characterization
of the immune-active pectin fractions of arr6 by further fractionation
of it by chromatographic means (Mélida et al. 2020). These analyses pointed to the
role of pentose-based oligosaccharides in triggering plant immune responses in arr6.
Specifically, we have identified pentose-based oligosaccharide structures, such
as beta-1,4-xylooligosaccharides, with specific degrees of polymerization carrying
arabinose decorations. Remarkably, these novel DAMPs, which trigger immune responses
in Arabidopsis, also activate immune responses in crops and confer enhanced disease
resistance to pathogens, including necrotrophic fungi (Mélida et al. 2020). The characterization of these new cell wall-derived
plant DAMPs represents the culmination of a long journey across novel mechanisms
of plant immunity in our lab that led us to determine the significant and specific
contribution of plant cell wall composition in disease resistance. This has been
a journey that we initiated with the necrotrophic fungus PcBMM and that has
taken us to the identification of novel, noncanonical, cell wall-mediated mechanisms
of immunity of relevance for different sets of pathogens. We sincerely guess
that our research can contribute to the development of innovative crop protection
technologies to reach the desire goal of more sustainable agriculture that will
feed the growing human population.
The June 2020
Editor’s pick for MPMI is “RNA Sequencing-Associated Study Identifies
GmDRR1 as Positively Regulating the Establishment of Symbiosis in
Soybean” with corresponding authors Dawei Xin and Qingshan Chen from the Northeast Agricultural
University in Harbin, China. To read more about Dawei you can find his bio here.
Study Identifies GmDRR1 as Positively Regulating the Establishment of
Symbiosis in Soybean
Dawei Xin and Qingshan Chen
Soybean is one of the most important
crops in the world, supplying protein and oil to humans and animals. Symbiosis
is a special characteristic of legumes that allows them to fix nitrogen from
the air. However, chemical nitrogen fertilization is still the main source utilized
in legume crops, which causes serious pollution in the environment. Too little
is understood about the mechanism of symbiosis, which impedes utilization of
symbiosis in agriculture. The benefits of symbiosis encourages us to become more
familiar with the molecular mechanism of legume–Rhizobium interaction.
The genes of Rhizobium sp. and host both play a pivotal role in
In recent decades, type Ⅲ effector (T3E) was found and identified as playing a pivotal role in
nodule formation. To date, there is no gene has been identified in a legume
host that directly interacts with T3E. Our lab has been working to identify the
genes that might interact with T3E and the soybean response mechanism to Rhizobium
spp. Considering the complex genetic background of soybean, we selected a genetic
population to identify the genes underlying symbiosis and the response to T3E.
Chromosome segment substituted lines (CSSL) with wild soybean genomic sequences
are an ideal genetic material to locate quantitative trait loci (QTL) and
mining genes in the target chromosome regions.
identify the chromosome region that might underlie symbiosis and the response
to T3E during symbiosis establishment, we screened the CSSL population, first
to compare the nodule-related phenotype and genotype of CSSL. After inoculation
with wild-type Rhizobium sp., two lines of CSSL were identified. One line
can form more nodules than the recurrent parent, and other can form fewer
nodules than the recurrent parent. This supports the hypothesis that
substituted chromosome segments play a role in the identified phenotype. The
substituted segments on the chromosome were detected by resequencing the genome
of two identified lines of CSSL and the recurrent parent.
Mining the response of
candidate genes to Rhizobium sp. and T3E
there are no single substituted segments on the chromosome, we needed to
identify the target region to reduce our workload. To accomplish this, we used
CSSL to map the QTL underlying nodule number after inoculation with a wild Rhizobium
sp. and derived T3E mutant. At the same time, RNA sequencing was performed to
detect the gene expression pattern located in the substituted segment of
chromosome. We used a wild-type Rhizobium sp. and T3E mutant strain to
inoculate the two identified CSSL lines and the recurrent parent. Many
different expression genes were found. To delimitate the region on the chromosome,
we used the QTL assistant to find the chromosome region. Because the length of
substituted segments can be identified by genomic resequencing and molecular
analysis, we can narrow down the chromosome region to a shortened region. This
was a great help to us in identifying the candidate for further work. Now,
several candidate genes that can interact with T3E have been identified, and we
have designed a more detailed experiment to elucidate the interaction
We are pleased that our work was accepted for publication by MPMI
and that we could share our findings with other researchers who we followed
during manuscript preparation.
We duly acknowledge funding from the Nature Science Foundation of China
and the graduate students of our lab at Northeast Agricultural University.
The July 2020 Editor’s pick for MPMI
infestans AVR2 Effector Escapes R2 Recognition Through Effector
Disordering,” in which Li-Na Yang and co-authors explore the role of intrinsic disorder in the development of
pathogenicity in the RXLR AVR2 effector of P. infestans. Their results
support the notion that intrinsic disorder is important for the effector
function of pathogens and demonstrate that SLiM-mediated protein–protein
interaction in the C-terminal effector domain might contribute greatly to the
evasion of resistance-protein detection in P. infestans.
Current Position: Associate professor
at the College of Plant Protection, Fujian Agriculture and Forestry University,
Education: B.Sc. and Ph.D. in Plant Pathology
at Fujian Agriculture and Forestry University, Fujian, China.
Non-scientific Interest: Traveling, walking, reading, gardening, and cooking.
Brief-bio: I am currently an associate professor at the College of Plant Protection,
Fujian Agriculture and Forestry University. I worked with Professor Jiasui
Zhan for nearly 10 years on the population genetics, molecular genetics, and
evolutionary ecology of the devastating potato pathogen Phytophthora infestans. I am interested in the effects of ecological
(biotic or abiotic) factors on the evolutionary potential and trajectory of
pathogen ecological and life history traits, such as fungicide resistance and pathogenicity governed by effector genes, etc. For
biotic factors, my research mainly
focuses on host diversification
and host resistance. We find
that compared with monoculture,
the mixture of different potato cultivars significantly slows down the evolution of pathogenicity
and fungicide resistance of P. infestans,
and late blight epidemic in the field is
also significantly reduced. This result
has been used to guide commercial production of potato in the Yunan and Guizhou
areas of Southwest China with great success. For abiotic factors, my research mainly focuses on the impacts of climate change, such as increasing atmosphere temperature
and carbon dioxide, on the evolution
of plant pathogens. We find temperature-mediated evolution of P. infestans in individual genes (e.g.
effector genes) and at the organism level. In the laboratory, P. infestans can adapt to changed
quickly, and the spatial differentiation of fungicide tolerance increases
under elevated experimental temperatures. We also find that the pathogenicity of P. infestans significantly increases as carbon dioxide
concentration increases. These results indicate late blight will become more difficult to control under future climate conditions of higher atmosphere temperatures and carbon dioxide concentrations.
Urooj is the lead author on a recent Editor's Pick paper in the MPMI journal. You can read the original article in the MPMI Journal here.
Current Position: PhD student at National Institute of Plant Genome Research (NIPGR), New Delhi, India
Education: BS and MS in biotechnology from C.S.J.M University, Kanpur, India
Non-scientific Interest: Cooking, interior designing, writing and mentoring personality development programs for women’s empowerment
Brief-bio: I am a doctoral student at NIPGR, working under the supervision of Dr. Muthappa Senthil-Kumar. The research work published in MPMI includes the side project undertaken during my PhD. The aim of this project was to identify the nonhost resistance (NHR) contributing genes and the mechanisms operating in a nonhost, chickpea (Cicer arietinum) plant against Alternaria brassicae, which is a devastating fungal pathogen that causes considerable yield loss in Brassica crops. For my PhD thesis I am working to understand the defense strategies used by Arabidopsis thaliana for limiting the nutrient availability to invading bacterial pathogens. Specifically, I am studying the role of SWEET class of transporters. I enjoyed working on these two projects that entails entirely different pathosystem that helped me in comprehending the broad scientific concepts and learning new techniques.
Urooj Fatima and Muthappa Senthil-Kumar; from the summary of the research Morpho-Pathological and Global Transcriptomic Analysis Reveals the Robust Nonhost Resistance Responses in Chickpea Interaction with Alternaria brassicae:
We have a few key points to share with the young researchers that we followed during manuscript preparation for submission in MPMI. A researcher must have a thorough understanding of their topic to carry out good research work. We have extensively studied the literature including recent and old research papers, review article and books related to my topic. Parallel to this manuscript, we wrote a review article about the perspective on the host and nonhost resistance mechanism against Alternaria blight. This allowed us to comprehend the topic of research better and to address the scientific problem systematically. Besides, it is important to note that the presentation of data in a well organized and comprehensive way is one of the primary factors to get a manuscript published in reputed journals. Apart from thorough experimentations, we critically worked on manuscript writing and data presentation in the form of quality figures. Further, data transparency is another important aspect in the research field. To provide more transparency, we have submitted the figure-wise raw data for the manuscript. It is advisable to submit the raw data files and make it available to reach the scientific audience to increase the credibility of your research work. By considering above mentioned points, we were able to publish our work in a highly reputed journal, MPMI.
Read more about how the project got started and Urooj Fatima and Muthappa Senthil-Kumar’s (National Institute of Plant Genome Research, New Delhi) thoughts on the research here.
Read the original article in the MPMI Journal
is the first article in a new series for IS-MPMI Interactions called InterConnections
(because it connects Interactions with the MPMI journal), where we will highlight first
authors of “Editor’s Pick” articles from the MPMI journal. The November “Editor’s Pick” is
“Mai1 Protein Acts Between Host Recognition of Pathogen Effectors andMitogen-Activated Protein Kinase Signaling”; the first author is Robyn Roberts
and the corresponding author is Gregory B. Martin.
This project is a demonstration of how persistence is
key to publication. Like many labs with “historical” projects that get passed
down from postgrad to postgrad, this particular project began about a decade
ago when Mai1 was discovered in a yeast-two-hybrid screen (by co-author Kerry
Pedley). Several postdocs and undergraduates contributed to the project over
the decade, but through the years, as people left the lab for other
opportunities, this project followed a postdoc chain until it landed on my
bench. With good timing between my other projects and the help of experienced
undergrads, I was able to contribute some key experiments that supported the
role and importance of Mai1 in NLR-triggered immunity (NTI).
I became interested in plant–microbe interactions
when I was an undergraduate researcher in Roger Innes’s lab at Indiana
University (IU), studying plant immunity in the arabidopsis–powdery mildew
system. I was really surprised at how knocking out single genes in plants could
have such drastic impacts on immunity. I found a lot of joy in working with
plants (and microbes) in research, and after earning my BS degree in biology at
IU, my interests in plant pathology led me to the University of Wisconsin–Madison,
where I earned my PhD in plant pathology. There, I studied the molecular
mechanisms of translation of a wheat virus, Triticum mosaic virus. While
I found viruses really fascinating and clever in how they package so much
information in their small genomes, I really wanted to move back to the plant
side to study plant defense. This led me to a postdoctoral position in Greg
Martin’s lab at the Boyce Thompson Institute (BTI) to work on tomato–bacterial
interactions with a focus on plant immunity.
I really like postdoc life. Without the pressures
of writing a thesis and facing a deadline to graduate, I can be more creative
in my research and have more diverse projects. Compared with graduate school, I
feel that I have a better handle on time management in the lab and have more
experience training undergraduate researchers, so I can accomplish more in less
time. I also really enjoy the opportunities to mentor students and work on my
own professional development, including my writing and transferrable skills
(soft skills). While there is sometimes more pressure to publish as a postdoc
than a graduate student, I find that most of this pressure is self-driven and
motivated by my desire to share my research with broader scientific audiences.
I participate in a number of extracurricular
activities, both professionally and as hobbies. Professionally, I am actively
involved in our BTI Postgraduate Society (PGS) and in scientific outreach. My
hobbies include volunteering with my dog in Cornell Companions at a local
nursing home, hiking around the Finger Lakes and in the Adirondacks, playing
saxophone, and crocheting. In graduate school, I was also a part of
deBary-tones, an outreach-based, plant pathology-themed band and received funds
from the APS Foundation and OPRO to record an album of our music (titled Faster
Than the Speed of Blight).