Studying Mitochondrial Structure and Function in &lt;em&gt;Drosophila&lt;/em&gt; Ovaries

Parker, Danitra; Moran, Aida; Mitra, Kasturi

doi:10.3791/54989-v

Cited by 3 publications

(2 citation statements)

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“…Because ovarian mitochondrial activity is directly related to oocyte maturation and oogenesis (Garcez et al, 2020; Parker et al, 2017; Sieber et al, 2016), we measured mitochondria potential in ovarioles from W1 and W2 flies by using the membrane potential dye TMRE normalized to a marker of mitochondrial mass, MitoTracker. Overall, mitochondrial membrane potential from W2 ovarioles was higher compared to W1 flies (Figure 3g,h).…”

Section: Resultsmentioning

confidence: 99%

Environmental microbes promote phenotypic plasticity in reproduction and sleep behaviour

et al. 2023

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The microbiome has been hypothesized as a driving force of phenotypic variation in host organisms that is capable of extending metabolic processes, altering development and in some cases, conferring novel functions that are critical for survival. Only a few studies have directly shown a causal role for the environmental microbiome in altering host phenotypic features. To assess the extent to which environmental microbes induce variation in host life‐history traits and behaviour, we inoculated axenic Drosophila melanogaster with microbes isolated from drosophilid populations collected from two different field sites and generated two populations with distinct bacterial and fungal profiles. We show that microbes isolated from environmental sites with modest abiotic differences induce large variation in host reproduction, fatty acid levels, stress tolerance and sleep behaviour. Importantly, clearing microbes from each experimental population removed the phenotypic differences. The results support the causal role of environmental microbes as drivers of host phenotypic plasticity and potentially, rapid adaptation and evolution.

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Section: Resultsmentioning

confidence: 99%

Environmental microbes promote phenotypic plasticity in reproduction and sleep behaviour

et al. 2023

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“…The ovaries were dissected and washed in Schneider's medium. The ovaries were immersed in Schneider's medium containing MitoSOX dye with a final concentration of 5 M for 15 min followed by a 5 min wash with Schneider's medium (Parker et al, 2017). The ovaries were immediately transferred to a glass slide and mounted using Schneider's medium for the imaging.…”

Section: Mitosox Staining For Mitochondrial Rosmentioning

confidence: 99%

Mitochondrial morphology dynamics and ROS regulate apical polarity and differentiation inDrosophilafollicle cells

Uttekar

Tomer

Rikhy

2023

Preprint

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Mitochondrial morphology dynamics regulate signaling pathways during epithelial cell formation and differentiation. The mitochondrial fission protein Drp1 affects the appropriate activation of EGFR and Notch signaling-driven differentiation of posterior follicle cells inDrosophilaoogenesis. The mechanisms by which Drp1 regulates epithelial polarity during differentiation are not known. In this study, we show that Drp1 depleted follicle cells are constricted in early stages and present in multiple layers at later stages with decreased levels of apical polarity protein aPKC. This defect is suppressed by additional depletion of mitochondrial fusion protein Opa1. Opa1 depletion leads to mitochondrial fragmentation and increased reactive oxygen species (ROS) in follicle cells. We find that increasing ROS by depleting the ROS scavengers, mitochondrial SOD2, and catalase also leads to mitochondrial fragmentation. Further, the loss of Opa1, SOD2, and catalase partially restores the defects in epithelial polarity and aPKC along with EGFR and Notch signaling in Drp1 depleted follicle cells. Our results show a crucial interaction between mitochondrial morphology, ROS generation, and epithelial cell polarity formation during the differentiation of follicle epithelial cells inDrosophilaoogenesis.

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Mitochondrial fusion and altered beta-oxidation drive muscle wasting in a Drosophila cachexia model

Dark,

Ali,

Golenkina

et al. 2024

EMBO Rep

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Cancer cachexia is a tumour-induced wasting syndrome, characterised by extreme loss of skeletal muscle. Defective mitochondria can contribute to muscle wasting; however, the underlying mechanisms remain unclear. Using a Drosophila larval model of cancer cachexia, we observed enlarged and dysfunctional muscle mitochondria. Morphological changes were accompanied by upregulation of beta-oxidation proteins and depletion of muscle glycogen and lipid stores. Muscle lipid stores were also decreased in Colon-26 adenocarcinoma mouse muscle samples, and expression of the beta-oxidation gene CPT1A was negatively associated with muscle quality in cachectic patients. Mechanistically, mitochondrial defects result from reduced muscle insulin signalling, downstream of tumour-secreted insulin growth factor binding protein (IGFBP) homologue ImpL2. Strikingly, muscle-specific inhibition of Forkhead box O (FOXO), mitochondrial fusion, or beta-oxidation in tumour-bearing animals preserved muscle integrity. Finally, dietary supplementation with nicotinamide or lipids, improved muscle health in tumour-bearing animals. Overall, our work demonstrates that muscle FOXO, mitochondria dynamics/beta-oxidation and lipid utilisation are key regulators of muscle wasting in cancer cachexia.

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Studying Mitochondrial Structure and Function in <em>Drosophila</em> Ovaries

Cited by 3 publications

References 0 publications

Environmental microbes promote phenotypic plasticity in reproduction and sleep behaviour

Environmental microbes promote phenotypic plasticity in reproduction and sleep behaviour

Mitochondrial morphology dynamics and ROS regulate apical polarity and differentiation inDrosophilafollicle cells

Mitochondrial fusion and altered beta-oxidation drive muscle wasting in a Drosophila cachexia model

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