Chapter 2 Intracellular Organelle Dynamics at nm Resolution

Author(s):  
Bhanu P. Jena
Plant Disease ◽  
2021 ◽  
Author(s):  
Xue Yang ◽  
Chun-Yan Gu ◽  
Yang Bai ◽  
Jia-Zhi Sun ◽  
Hao-Yu Zang ◽  
...  

Pomegranate crown rot caused by Coniellagranati is one of the most severe diseases of pomegranate. To date, no fungicides have been registered for controlling this disease in China. Pyraclostrobin, belonging to strobilurin fungicides, has a broad spectrum of activity against many phytopathogens. In this study, based on the mycelial growth and conidial germination inhibition methods, we investigated the biological activity of pyraclostrobin against C. granati at the presence of 50 μg/mL SHAM using 80 isolates collected from different orchards in China during 2012-2018. The EC50 (50% effective concentration) values ranged from 0.040-0.613 μg/mL for mycelial growth and 0.013-0.110 μg/mL for conidium germination, respectively. Treated with pyraclostrobin, the hyphae morphology changed and conidial production of C. granati decreased significantly. The result of transmission electron microscope showed that treatment of pyraclostrobin could make the cell wall thinner, and lead to ruptured cell membrane and formation of intracellular organelle autophagosomes. The pyraclostrobin showed good protective and curative activities against C. granati on detached pomegranate fruits. In field trials, pyraclostrobin showed excellent control efficacy against this disease in which the treatment of 25% pyraclostrobin EC 1000× provided 92.25% and 92.58% control efficacy in 2019 and 2020, respectively, significantly higher than that of other treatments. Therefore, pyraclostrobin could be a candidate fungicide for the control of pomegranate crown rot.


Author(s):  
Vishnu K. Kumar ◽  
Atreju Lackey ◽  
Jonathan Snyder ◽  
Sunil Karhadkar ◽  
Ajay D. Rao ◽  
...  

Research efforts in the twenty-first century have been paramount to the discovery and development of novel pharmacological treatments in a variety of diseases resulting in improved life expectancy. Yet, cardiac disease remains a leading cause of morbidity and mortality worldwide. Over time, there has been an expansion in conditions such as atrial fibrillation (AF) and heart failure (HF). Although past research has elucidated specific pathways that participate in the development of distinct cardiac pathologies, the exact mechanisms of action leading to disease remain to be fully characterized. Protein turnover and cellular bioenergetics are integral components of cardiac diseases, highlighting the importance of mitochondria and endoplasmic reticulum (ER) in driving cellular homeostasis. More specifically, the interactions between mitochondria and ER are crucial to calcium signaling, apoptosis induction, autophagy, and lipid biosynthesis. Here, we summarize mitochondrial and ER functions and physical interactions in healthy physiological states. We then transition to perturbations that occur in response to pathophysiological challenges and how this alters mitochondrial–ER and other intracellular organelle interactions. Finally, we discuss lifestyle interventions and innovative therapeutic targets that may be used to restore beneficial mitochondrial and ER interactions, thereby improving cardiac function.


2009 ◽  
Vol 56 (Supplement) ◽  
pp. 312-317 ◽  
Author(s):  
Kenichi Ishibashi ◽  
Shin Koike ◽  
Shintaro Kondo ◽  
Shigeki Hara ◽  
Yasuko Tanaka

2020 ◽  
Vol 13 (2) ◽  
Author(s):  
Wenjing Li ◽  
Shuhao Zhang ◽  
Ge Yang

2011 ◽  
Vol 11 ◽  
pp. 2364-2381 ◽  
Author(s):  
Oliver Nüsse

Phagocytes are specialized cells of the immune system, designed to engulf and destroy harmful microorganisms inside the newly formed phagosome. The latter is an intracellular organelle that is transformed into a toxic environment within minutes and disappears once the pathogen is destroyed. Reactive oxygen species and reactive nitrogen species are produced inside the phagosome. Intracellular granules or lysosomes of the phagocyte fuse with the phagosome and liberate their destructive enzymes. This process of phagocytosis efficiently protects against most infections; however, some microorganisms avoid their destruction and cause severe damage. To understand such failure of phagosomal killing, we need to learn more about the actual destruction process in the phagosome. This paper summarizes methods to investigate the biochemistry of the phagosome and discusses some of their limitations. In accordance with the nature of the phagosome, the issue of localization and temporal dynamics is emphasized, and recent developments are highlighted.


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