Inhibition of axon regeneration: unexpected roles of piRNA and NAD+ pa…
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- Writer 최고관리자
- 2017-11-28
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[BK21 Plus Seminar]
▶Subject: Inhibition of axon regeneration: unexpected roles of piRNA and NAD+ pathways
▶Speaker: KYUNG WON KIM, Ph.D. (Assistant project scientist, University of California at San Diego)
▶Date: 4:00PM/Dec, 11(Mon.)/2017
▶Place: Life Science Bldg. #104
▶Abctract
Axon regeneration after nerve injury, which is key for functional recovery, is a conserved biological process in many animals. Genetic analysis in Caenorhabditis elegans has played a significant role in identifying conserved regeneration pathways. Here I report unexpected roles for two highly conserved pathways in C. elegans axon regrowth. One involves the nicotinamide mononucleotide adenylyltransferase (NMNAT) enzyme, which catalyzes a vital step in nicotinamide adenine dinucleotide (NAD+) biosynthesis and confers neuroprotection in many organisms. I found that C. elegans NMNAT inhibits axon regeneration dependent on its enzymatic activity for NAD+ production. The second inhibitory pathway involves the PIWI-interacting small non-coding RNA (piRNA) pathway. I found that loss of function in a subset of components of the piRNA pathway results in enhanced axon regrowth. Essential piRNA factors inhibit axon regeneration in a cell-autonomous manner in neurons. While this finding is surprising because piRNA pathway has long been thought to function solely in the germline, my work shows an example of its somatic/neuronal role. I will investigate further to better understand these unexpected axon regeneration mechanisms, which should contribute to the functional recovery after brain damage.
▶Inquiry: Prof. Seung-Jae Lee (279-2351)
* This seminar will be given in English.
Please refrain from taking photos during seminars. *
▶Subject: Inhibition of axon regeneration: unexpected roles of piRNA and NAD+ pathways
▶Speaker: KYUNG WON KIM, Ph.D. (Assistant project scientist, University of California at San Diego)
▶Date: 4:00PM/Dec, 11(Mon.)/2017
▶Place: Life Science Bldg. #104
▶Abctract
Axon regeneration after nerve injury, which is key for functional recovery, is a conserved biological process in many animals. Genetic analysis in Caenorhabditis elegans has played a significant role in identifying conserved regeneration pathways. Here I report unexpected roles for two highly conserved pathways in C. elegans axon regrowth. One involves the nicotinamide mononucleotide adenylyltransferase (NMNAT) enzyme, which catalyzes a vital step in nicotinamide adenine dinucleotide (NAD+) biosynthesis and confers neuroprotection in many organisms. I found that C. elegans NMNAT inhibits axon regeneration dependent on its enzymatic activity for NAD+ production. The second inhibitory pathway involves the PIWI-interacting small non-coding RNA (piRNA) pathway. I found that loss of function in a subset of components of the piRNA pathway results in enhanced axon regrowth. Essential piRNA factors inhibit axon regeneration in a cell-autonomous manner in neurons. While this finding is surprising because piRNA pathway has long been thought to function solely in the germline, my work shows an example of its somatic/neuronal role. I will investigate further to better understand these unexpected axon regeneration mechanisms, which should contribute to the functional recovery after brain damage.
▶Inquiry: Prof. Seung-Jae Lee (279-2351)
* This seminar will be given in English.
Please refrain from taking photos during seminars. *
