앞줄 좌측 두번째 이상아 학생, 세번째 차선주 학생

 

지난 12일 서울 코엑스에서 2016년도 한국분자세포생물학회 정기학술대회가 개최되었다. 본 학술대회는 한국분자세포생물학회에서 주관하여 매년 가을에 개최되는 국제학술대회로, 회원 수 약 1만 2500명의 국내 생명과학분야 최대 규모의 학회이다. 이번 학술대회에서는 총 1012편의 논문 중 단 71편의 포스터만 우수 포스터로 선정되었으며, 순천향대학교에서는 의생명연구원 의생명융합학과 소속 석박사통합과정 이상아(지도교수: 이만렬), 석사과정 차선주(지도교수: 김기영) 학생이 수상하였다.

이상아 학생은 ‘미토콘드리아 대사를 통해 역분화(reprogramming) 효율을 조절하는 새로운 microRNA 대한 연구’에서 체세포에서 유도만능줄기세포(iPS cell)로 역분화 될 때 미토콘드리아 유전자 및 대사를 직접 조절하는 microRNA를 밝혀 그에 대한 새로운 역분화 기전을 규명하였으며, 차선주 학생은 ‘루게릭병 발병 과정에 관여하는 새로운 조절 인자의 발굴에 관한 연구’에서 GstO 유전자가 루게릭병의 발병 원인 단백질로 알려진 FUS의 세포 내 응집과정을 억제함으로써 발병과정을 조절한다는 사실을 초파리 모델을 통해 규명하여 이를 통한 신규 치료제 발굴 가능성을 제시하였다 

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이상아 학생

MiR-31/SDHA Axis Regulates Reprogramming Efficiency through Mitochondrial Metabolism

Metabolism is remodeled when somatic cells are reprogrammed into induced pluripotent stem cells (iPSCs), but the majority of iPSCs are not fully reprogrammed. In a shift essential for reprogramming, iPSCs use less mitochondrial respiration but increased anaerobic glycolysis for bioenergetics. We found that microRNA 31 (miR-31) suppressed succinate dehydrogenase complex subunit A (SDHA) expression, vital for mitochondrial electron transport chain (ETC) complex II. MiR-31 overexpression in partially reprogrammed iPSCs lowered SDHA expression levels and oxygen consumption rates to that of fully reprogrammed iPSCs, but did not increase the proportion of fully reprogrammed TRA1-60+ cells in colonies unless miR-31 was co-transduced with Yamanaka factors, which resulted in a 2.7-fold increase in full reprogramming. Thus switching from mitochondrial respiration to glycolytic metabolism through regulation of the miR-31/SDHA axis is critical for lowering the reprogramming threshold. This is supportive of multi-stage reprogramming whereby metabolic remodeling is fundamental.

차선주 학생

Novel Regulator Involved in the Pathogenesis of Amyotrophic Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is devastating fatal neurodegenerative disease which characterized by progressive and selective degeneration of both upper and lower motor neurons. Recently some kinds of ALS causing genes, TDP-43, FUS, TAF15, are identified in yeast system. Molecular mechanisms of ALS pathogenesis are not yet fully understood. Therefore, we want to find novel regulators and investigate pathogenic mechanism of ALS using Drosophila model. First we found that GstO gene is genetically interacts with FUS-induced ALS model in our genetic modifier screening. GstO overexpression alleviates some of the FUS-induced defective phenotypes such as locomotive activity, life-span, neuromuscular junctional defect. Furthermore, we show that expression level of FUS is decreased in cytoplasmic fraction of GstO co-expressing flies. Moreover, GstO decreased FUS accumulation in cytoplasm by enhancing the protein solubility of FUS. These results suggest that the GstO has a protective role in FUS-induced ALS.