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Insects exhibit diverse physiological processes by undergoing metamorphosis with enormous reproductive potential. Temperature and nutrients allow the insect to grow and reach to a certain level of critical body size. This growth is mainly mediated by insulin hormone signal in insects. In contrast, juvenile hormone (JH) and 20-hydroxyecdysone (20E) mediate endocrine signals to timely control the metamorphosis.
Our lab has investigated the roles of various endocrine signals in insect physiological processes. Currently, we are focusing on eicosanoid signaling mediating insect immune and reproductive processes. Eicosanoids are C20 polyunsaturated fatty acids oxygenated by various oxygenase enzymes. These eicosanoids include prostaglandins (PGs), leukotrienes (LTs), and epoxyeicosatrienoic acids (EETs).
One of the main precursors of the eicosanoid biosynthesis is arachidonic acid (AA, C20:4). However, little AA is present in insect phospholipids. Thus most scientists in this field are not sure that eicosanoids mediate insect physiological processes. Ariful Hasan (MS degree at 2019) discovered the biosynthetic pathway from linoleic acid (C18:2) to AA (IBMB, 2019).
Dr. Seyedeh Minoo Sajjadian (postdoctoral associate) continued the discovery to investigate the role of prostaglandins (PGs) in gut immunity (Open Biology, 2020). Pathogen infection triggers eicosanoid biosynthesis and induce PG signaling to produce reactive oxygen species (ROS). These ROS molecules are synthesized by double oxidase (Duox). PGE2 stimulate Duox expression in S. exigua.
Ahmed Shabbir (MS degree at 2019, now research associate) unravel the PGE2 signaling involved in modulating hemocyte behaviors of S. exigua in response to immune challenge. Different entomopathogenic bacteria classified into Xenorhabdus and Photorhabdus were different in inhibition of phospholipase A2 (PLA2) enzyme activity leading to eicosanoid biosynthesis. Variation in the enzyme inhibitory activity was positively associated with suppression of cellular immune responses by preventing eicosanoid biosynthesis and ultimately determined the potency of bacterial virulence. Among eicosanoids, PGE2 played crucial role in mediating hemocyte-spreading behavior by activating cytoskeletal rearrangement via F-actin growth. In the process of hemocyte-spreading behavior, aquaporin (water-transporting pore channel) activity was required for increasing local cell volume and functionally associated with PGE2 signal in S. exigua. Furthermore, PGE2 was able to mediate hemocyte-spreading behavior via an actin polymerization and bundling proteins. Specific inhibitors or RNA interference (RNAi) against trimeric or small G proteins also blocked the PGE2 mediation of hemocyte-spreading behavior. A specific PGE2 receptor has been identified and its heterologous expression in Sf9 cells was specifically responsive to PGE2 to activate cAMP production. Knock-out mutant of PGE2 receptor using CRISPR-Cas9 suffered from larval development and resulted in high immature mortality along with miniature adults. Finally, this study identified PGE2 synthase gene (Se-PGES2) in S. exigua. Se-PGES2 was predicted to possess all active sites for catalyzing isomerization from PGH2 to PGE2. RNAi of Se-PGES2 expression led to severe immunosuppression of S. exigua. On the other hand, overexpression of Se-PGES2 was induced by in vivo transient expression (IVTE) in S. exigua. IVTE of Se-PGES2 significantly up-regulated immune responses to be tolerant against entomopathogens. However, the uncontrolled and excess PGE2 production resulted in fitness cost such as retarded larval development and reduced egg production.
Dr. Mohammad Vatanparast (postdoctoral associate) is an expert in CRISPR-Cas9 technology to generate mutant line to address the role of PLA2 in insect physiological processes.
Roy Chandra Miltan (PhD candidate) is assessing calcium signaling in response to immune challenge. He recently found thromboxane B2 mediates hemocyte aggregation around fungal pathogen (Metarhizium rileyi).
Md Mahi Imam Mollah (PhD candidate) has discovered the first insect DAMP molecule. It is called HMG-like DSP1. It is localized in nucleus, but translocates to outside cells to trigger immune signal.
Choi, Dooyeol (MS student) has interest in medical entomology. His model insect is Asian tiger mosquito (Aedes albopictus) transmitting various arboviruses. His recent research is to identify PLA2 genes from this insect and investigate the mosquito reproduction.
Chulyoung Kim has interests in immune responses to defend microbial pathogens. Especially, insects live in relatively dirty environments presumably rich in microbes including bacteria, fungi and viruses. Thus, insects survive and develop by defeating the continuous infections from the pathogenic microbes. Interestingly, some thrips live along with pathogenic viruses and exhibit a special symbiotic life patterns. How is it possible?
Here is a famous insect pest called western flower thrips (WFT), Frankliniella occidentalis. WFT is a vector transferring plant virus called tomato spotted wilt virus (TSWV), which causes devastating crop damage over the world. First, I have an interest in how the thrips picks up and multiplies TSWV in its internal body. There must be an immune defense from WFT against TSWV. In other way, TSWV may suppress WFT immune responses to protect from the antiviral responses. Second, are there any volatile signal from TSWV to attract WFT? If I identify the attractive signal, I can use the chemical to attract and kill the thrips without use of chemical insecticides. Finally, there are several semiochemicals identified from WFT for aggregation pheromone, trail pheromone, and alarm pheromone. Can I optimally integrate these semiochemicals to distrupt the communication of WFT populations for mass trapping?
KiWon's research interest is controlling mosquitoes using microbial pesticides. Currently, I prepare a bacterial toxin originated from Bacillus thuringiensis subsp. israelensis (BtI). I assume this bacterial Cry toxin disintegrates the mosquito midgut. Once the midgut epithelium is damaged, the gut microbes can get access to the mosquito hemocoel and cause fatal septicemia. Following is a mosquito (한국숲모기, Aedes koreicus) that I culture for my interesting study.
I(Tafim) joined this lab to study molecular biology and its related technologies. Currently I am working with expression analysis of an immune-associated gene called Repat33. Actually, Repat33 is one of Repat gene family consisting more than 40 members. Repat33 is highly inducible gene in response to various microbial pathogens. Loss-of-function of Repat33 using RNA interference technique led to the test insects under significant immunosuppression. Interestingly, Repat33 expression is under control of eicosanoids. Thus, pathogen infection induces eicosanoid immune signaling pathway, which up-regulates Repat33 expression. However, we do not know how Repat33 mediates both cellular and humoral immune responses. One clue is coming from a bioinformatics analysis with a collaboration with Ahmed Shabbir. Repat33 possesses its C-terminal MBF2 motif. This suggests its role as a coactivator by linking immunity-specific transcriptional factor (such as FTZ-F1 or NFkB) to general transcriptional factor (TFIIA). I look for this functional possibility and continue my research efforts to address this hypothesis
2021.April 02 Cherry Blossom!!!!!!!!
We are real Plant Doctor!!!!!! on 12 April & 29 April
Wow ~~~~ Handsome Guys!!!!!!! on Spring Conference
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