Functional remodeling of adrenal steroidogenic tissue by food deprivation in the lizard, Sceloporus undulatus

Author(s):  
Rocco V. Carsia ◽  
Patrick J. McIlroy ◽  
Christine A. Duncan ◽  
Henry B. John-Alder
2012 ◽  
Vol 60 (S 01) ◽  
Author(s):  
EM Delmo Walter ◽  
H Siniawski ◽  
T Komoda ◽  
R Hetzer

Animals ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2200
Author(s):  
Ruben X. G. Silva ◽  
Paulo Cartaxana ◽  
Ricardo Calado

Berghia stephanieae is a stenophagous sea slug that preys upon glass anemones, such as Exaiptasia diaphana. Glass anemones host photosynthetic dinoflagellate endosymbionts that sea slugs ingest when consuming E. diaphana. However, the prevalence of these photosynthetic dinoflagellate endosymbionts in sea slugs appears to be short-lived, particularly if B.stephanieae is deprived of prey that host these microalgae (e.g., during bleaching events impacting glass anemones). In the present study, we investigated this scenario, along with food deprivation, and validated the use of a non-invasive and non-destructive approach employing chlorophyll fluorescence as a proxy to monitor the persistence of the association between sea slugs and endosymbiotic photosynthetic dinoflagellates acquired through the consumption of glass anemones. Berghia stephanieae deprived of a trophic source hosting photosynthetic dinoflagellate endosymbionts (e.g., through food deprivation or by feeding on bleached E. diaphana) showed a rapid decrease in minimum fluorescence (Fo) and photosynthetic efficiency (Fv/Fm) when compared to sea slugs fed with symbiotic anemones. A complete loss of endosymbionts was observed within 8 days, confirming that no true symbiotic association was established. The present work opens a new window of opportunity to rapidly monitor in vivo and over time the prevalence of associations between sea slugs and photosynthetic dinoflagellate endosymbionts, particularly during bleaching events that prevent sea slugs from incorporating new microalgae through trophic interactions.


2021 ◽  
Vol 22 (8) ◽  
pp. 4167
Author(s):  
Xiaonan Sun ◽  
Jalen Alford ◽  
Hongyu Qiu

Mitochondria undergo structural and functional remodeling to meet the cell demand in response to the intracellular and extracellular stimulations, playing an essential role in maintaining normal cellular function. Merging evidence demonstrated that dysregulation of mitochondrial remodeling is a fundamental driving force of complex human diseases, highlighting its crucial pathophysiological roles and therapeutic potential. In this review, we outlined the progress of the molecular basis of mitochondrial structural and functional remodeling and their regulatory network. In particular, we summarized the latest evidence of the fundamental association of impaired mitochondrial remodeling in developing diverse cardiac diseases and the underlying mechanisms. We also explored the therapeutic potential related to mitochondrial remodeling and future research direction. This updated information would improve our knowledge of mitochondrial biology and cardiac diseases’ pathogenesis, which would inspire new potential strategies for treating these diseases by targeting mitochondria remodeling.


2021 ◽  
Vol 177 ◽  
pp. 183-190
Author(s):  
Danielle Edmunds ◽  
Stuart Wigby ◽  
Jennifer C. Perry

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