• 제목/요약/키워드: starvation response

검색결과 63건 처리시간 0.026초

Impact of inhibitors of amino acid, protein, and RNA synthesis on C allocation in the diatom Chaetoceros muellerii: a FTIR approach

  • Giordano, Mario;Norici, Alessandra;Beardall, John
    • ALGAE
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    • 제32권2호
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    • pp.161-170
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    • 2017
  • Fourier Transform Infrared (FTIR) spectroscopy was used to study carbon allocation patterns in response to N-starvation in the nearly ubiquitous diatom Chaetoceros muellerii. The role of gene expression, protein synthesis and transamination on the organic composition of cells was tested by using specific inhibitors. The results show that inhibition of key processes in algal metabolism influence the macromolecular composition of cells and and prior cell nutritional state can influence a cell's response to changing nutrient availability. The allocation of C can thus lead to different organic composition depending on the nutritional context, with obvious repercussions for the trophic web. This also shows that C allocation in algal cells is highly flexible and that C (and the energy associated with its allocation) can be variably and rapidly partitioned in algal cells in response to relatively short term perturbations. Furthermore, the data confirm and extend the utility of infrared spectroscopy as a probe of the metabolic state of autotrophic cells.

Bacillus subtilis와 Listeria monocytogenes의 일반 스트레스반응의 비교 (Comparison of the ${\sigma}^B$-Dependent General Stress Response between Bacillus subtilis and Listeria monocytogenes)

  • 신지현
    • 미생물학회지
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    • 제45권1호
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    • pp.10-16
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    • 2009
  • 일부 그람양성세균들은 고온, 저온, 염, 에탄올, 산소와 영양분 고갈과 같은 다양한 스트레스 상태에 노출되면, 일반 스트레스반응(general stress response)에 의해서 일련의 스트레스 단백질군을 발현시켜 외부 스트레스를 극복하고 세균의 생존력을 증가시킨다. 비병원성균인 Bacillus subtilis의 일반 스트레스반응에 관해서는 많은 연구가 이루어져 있으므로 다른 균의 연구모델로 이용이 가능하다. 본 총설에서는 B. subtilis와 병원성균인 Listeria monocytogenes의 일반 스트레스반응의 유사성과 차이점을 B. subtilis를 모델로 하여 비교하였다. 두 균의 일반 스트레스반응은 대체 전사 인자인 ${\sigma}^B$ (alternative transcription factor sigma B)에 의해서 조절되고 신호전달 네트워크 또한 매우 유사하며, ${\sigma}^B$ 의존성 유전자들에 의해 150여 개의 스트레스 단백질들이 발현된다. 그러나 L. monocytogenes는 B. subtilis의 에너지 스트레스 신호 경로를 가지고 있지 않은 점과, 일반 스트레스반응에 의해 병독 유전자들(virulence genes)이 조절되는 것이 가장 큰 차이점이다. 그러므로 L. monocytogenes의 생리 및 병원성 규명을 위해서는 일반 스트레스반응에 관한 이해가 매우 중요하다.

적조발생시기 참돔의 절식과 사육밀도에 따른 성장과 혈액성상 (Growth and Blood Characteristics of Red Sea Bream Pagrus major by Starvation and Stocking Density during Red Tide)

  • 김원진;이정용;신윤경;원경미
    • 한국어류학회지
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    • 제30권4호
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    • pp.194-204
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    • 2018
  • 본 연구는 매년 C. polykrikoides 적조에 의해 발생하는 양식 어류 폐사의 피해를 최소화하기 위해 적조시기 참돔의 절식과 밀도의 영향을 조사하였다. 해상가두리($11m{\times}11m{\times}5m$)에서 섭식-고밀도(F-HD), 절식-고밀도(S-HD), 절식-저밀도(S-LD) 세 그룹으로 구분하여 5주간의 절식 후 4주간의 먹이공급을 통해 참돔의 생존율, 성장, 성장회복 그리고 혈액학적 변화를 조사한 결과, 생존율은 F-HD에서 85.5%로 가장 낮았고, S-LD는 97.3%로 높은 생존율을 보였다. 5주간의 절식기간 동안 두절식구는 전장, 체중 성장률에서 마이너스 성장을 보여 섭식구와 유의한 차이를 보였다(P<0.05). 하지만 먹이 재공급 후두 절식구 모두 성장회복을 보였다. 특히 S-LD는 먹이 재공급 기간 동안 빠른 성장회복을 통해 보상성장 경향을 보였으며, 섭식구와 유의한 차이를 나타냈다(P<0.05). ALB, TCHO, TP, TG 혈액분석을 통한 실험구의 영양상태는 절식구에서 섭식구에 비해 유의하게 감소하였지만 먹이 공급 후 실험개시 시 수준으로 빠르게 회복하였다. 스트레스와 생리활성 지표인 Ht, Hb, AST, ALT 그리고 GLU가 적조 노출 후 F-HD에서 동일한 시기에 급격히 상승하여, 적조시기 섭식, 고밀도 사육환경은 양식어류에게 더 민감한 사육환경으로 작용할 것으로 여겨진다. 따라서 본 연구의 적조시기 절식과 밀도에 따른 생존율, 성장회복, 혈액성상을 통한 결과를 토대로, 적조 노출에 따른 절식과 밀도 조절이 사육어류 관리방안을 위한 기초자료로 활용될 수 있을 것이다.

NCQ와 입출력 스케줄러의 기대 불일치로 인한 입출력 요청의 굶주림 현상 제거 (Eliminating Request Starvation due to Expectation Discrepancy between NCQ and I/O Scheduler)

  • 유영진;신동인;정임영;염헌영
    • 한국정보과학회논문지:컴퓨팅의 실제 및 레터
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    • 제15권5호
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    • pp.400-404
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    • 2009
  • Native Command Queueing(이하 NCQ)는 디스크 드라이브 내의 명령어 큐에 존재하는 요청들의 순서를 재조정하여 throughput을 최대화하는 기술이다. NCQ는 최신 S-ATA 2의 표준 스펙에 포함되었고, 다수의 디스크 벤더들이 자사의 디스크 모델에 이를 구현하고 있다. 하지만 이 새로운 기술이 운영체제와 디스크 드라이브간의 정보 차이를 유발할 가능성이 있다. 운영체제는 자신이 지시한 순서대로 디스크가 입출력 요청을 서비스할 것이라 생각하지만, NCQ가 지원되는 디스크는 이를 무시하고 throughput을 최대화할 목적으로만 요청을 처리할 것이다. 이것을 기대 불일치라 부를 수 있다. 이로 인해 성능에 이상한 현상이 발생하거나, 입출력 요청이 심각하게 굶주릴 가능성이 있다. 본 논문에서는 기대 불일치로 인한 입출력 요청의 굶주림 현상을 실제로 확인하고, 이를 해결하기 위한 해결책을 제시한다. 이 해결책은 간단하고, 특별한 하드웨어의 추가나 변경을 요구하지 않으며, 이식성이 좋다. 이를 실험 결과를 통해 확인하도록 한다.

Energy Metabolism in Human Pluripotent Stem and Differentiated Cells Compared Using a Seahorse XF96 Extracellular Flux Analyzer

  • Hyun Kyu Kim;Yena Song;Minji Kye;Byeongho Yu;Sang Beom Park;Ji Hyeon Kim;Sung-Hwan Moon;Hyungkyu Choi;Jong-Seok Moon;Jae Sang Oh;Man Ryul Lee
    • International Journal of Stem Cells
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    • 제17권2호
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    • pp.194-203
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    • 2024
  • Evaluating cell metabolism is crucial during pluripotent stem cell (PSC) differentiation and somatic cell reprogramming as it affects cell fate. As cultured stem cells are heterogeneous, a comparative analysis of relative metabolism using existing metabolic analysis methods is difficult, resulting in inaccuracies. In this study, we measured human PSC basal metabolic levels using a Seahorse analyzer. We used fibroblasts, human induced PSCs, and human embryonic stem cells to monitor changes in basal metabolic levels according to cell number and determine the number of cells suitable for analysis. We evaluated normalization methods using glucose and selected the most suitable for the metabolic analysis of heterogeneous PSCs during the reprogramming stage. The response of fibroblasts to glucose increased with starvation time, with oxygen consumption rate and extracellular acidification rate responding most effectively to glucose 4 hours after starvation and declining after 5 hours of starvation. Fibroblasts and PSCs achieved appropriate responses to glucose without damaging their metabolism 2~4 and 2~3 hours after starvation, respectively. We developed a novel method for comparing basal metabolic rates of fibroblasts and PSCs, focusing on quantitative analysis of glycolysis and oxidative phosphorylation using glucose without enzyme inhibitors. This protocol enables efficient comparison of energy metabolism among cell types, including undifferentiated PSCs, differentiated cells, and cells undergoing cellular reprogramming, and addresses critical issues, such as differences in basal metabolic levels and sensitivity to normalization, providing valuable insights into cellular energetics.

Evaluation of apoptosis after ionizing radiation in feeding and starving rats

  • Lee, Jae-Hyun;Cho, Kyung-Ja;Hong, Seok-Il;Park, Min-Kyung
    • 한국수의병리학회지
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    • 제2권1호
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    • pp.37-46
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    • 1998
  • It has been known that $\gamma$-irradiation usually induces cell death in regenerating stem cell in normal tissues like skin, intestine and hematopoietic organ. The experiment were carried out to evaluate the early response of radiation injury in radiosensitive and intermediate radiosensitive tissues in feeding and starving rats with the doses of 3.5 and 7.0 Gy. The results of the study showed that the histological phenomenon was apoptosis in the doses of the radiation as the early response of tissue injury. Apoptosis were showed organ-specific and cellular specific responses suggesting that the selection of apoptosis be exactly focused on highly renewal organs and cells. It was interesting that the rats starved for 72 hours prior to irradiation induced less apoptosis in liver than fed rats. As for cellular responses it appeared that apoptotic cells were mostly distributed in ductal or periportal cells in liver of feeding rats unlikely in liver of Starving rots which showed no difference in zonal distribution. In salivary gland apoptotic cells in fed rats were highly induced in intercalating and ductal cell population than in acinar cell population although unlikely in starved rats. This study showed the value of apoptosis using the detection system of TUNEL for evaluating cellular damage after radiation injury and the diminished effect of starvation on cell damage after ionizing irradiation.

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Autophagy down-regulates NLRP3-dependent inflammatory response of intestinal epithelial cells under nutrient deprivation

  • Yun, Yewon;Baek, Ahruem;Kim, Dong-Eun
    • BMB Reports
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    • 제54권5호
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    • pp.260-265
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    • 2021
  • Dysregulation of inflammation induced by noninfectious stress conditions, such as nutrient deprivation, causes tissue damage and intestinal permeability, resulting in the development of inflammatory bowel diseases. We studied the effect of autophagy on cytokine secretion related to intestinal permeability under nutrient deprivation. Autophagy removes NLRP3 inflammasomes via ubiquitin-mediated degradation under starvation. When autophagy was inhibited, starvation-induced NLRP3 inflammasomes and their product, IL-1β, were significantly enhanced. A prolonged nutrient deprivation resulted in an increased epithelial mesenchymal transition (EMT), leading to intestinal permeability. Under nutrient deprivation, IL-17E/25, which is secreted by IL-1β, demolished the intestinal epithelial barrier. Our results suggest that an upregulation of autophagy maintains the intestinal barrier by suppressing the activation of NLRP3 inflammasomes and the release of their products, including pro-inflammatory cytokines IL-1β and IL-17E/25, under nutrient deprivation.

Inhibitory Role of TRIP-Br1/XIAP in Necroptosis under Nutrient/Serum Starvation

  • Sandag, Zolzaya;Jung, Samil;Quynh, Nguyen Thi Ngoc;Myagmarjav, Davaajargal;Anh, Nguyen Hai;Le, Dan-Diem Thi;Lee, Beom Suk;Mongre, Raj Kumar;Jo, Taeyeon;Lee, MyeongSok
    • Molecules and Cells
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    • 제43권3호
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    • pp.236-250
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    • 2020
  • Currently, many available anti-cancer therapies are targeting apoptosis. However, many cancer cells have acquired resistance to apoptosis. To overcome this problem, simultaneous induction of other types of programmed cell death in addition to apoptosis of cancer cells might be an attractive strategy. For this purpose, we initially investigated the inhibitory role of TRIP-Br1/XIAP in necroptosis, a regulated form of necrosis, under nutrient/serum starvation. Our data showed that necroptosis was significantly induced in all tested 9 different types of cancer cell lines in response to prolonged serum starvation. Among them, necroptosis was induced at a relatively lower level in MCF-7 breast cancer line that was highly resistant to apoptosis than that in other cancer cell lines. Interestingly, TRIP-Br1 oncogenic protein level was found to be very high in this cell line. Up-regulated TRIP-Br1 suppressed necroptosis by repressing reactive oxygen species generation. Such suppression of necroptosis was greatly enhanced by XIAP, a potent inhibitor of apoptosis. Our data also showed that TRIP-Br1 increased XIAP phosphorylation at serine87, an active form of XIAP. Our mitochondrial fractionation data revealed that TRIP-Br1 protein level was greatly increased in the mitochondria upon serum starvation. It suppressed the export of CypD, a vital regulator in mitochondria-mediated necroptosis, from mitochondria to cytosol. TRIP-Br1 also suppressed shikonin-mediated necroptosis, but not TNF-α-mediated necroptosis, implying possible presence of another signaling pathway in necroptosis. Taken together, our results suggest that TRIP-Br1/XIAP can function as onco-proteins by suppressing necroptosis of cancer cells under nutrient/serum starvation.