Biosystematic Studies in the Bouteloua curtipendula Complex. IV. Dynamics of Variation in B. curtipendula var. caespitosa

1964 ◽  
Vol 91 (6) ◽  
pp. 465 ◽  
Author(s):  
Z. J. Kapadia ◽  
F. W. Gould
Keyword(s):  
Bouteloua Curtipendula ◽  
Complex Iv

EMBRIOGÉNESIS SOMÁTICA INDUCIDA CON ESTRÉS OSMÓTICO EN Bouteloua curtipendula (Michx.) Torr., ESPECIE RECALCITRANTE Y APOMÍCTICA

2015 ◽  
Vol 38 (4) ◽  
pp. 359
Author(s):  
Álvaro Bernal-Flores ◽  
Adrián R. Quero-Carrillo ◽  
Alejandrina Robledo-Paz ◽  
H. Araceli Zavaleta-Mancera ◽  
Paulino Pérez-Rodríguez
Keyword(s):  
Bouteloua Curtipendula

En el presente estudio varios medios de cultivo con diferentes auxinas fueron establecidos para la regeneración de plantas normales en pasto Banderita Bouteloua curtipendula (Michx.) Torr., a partir de callos inducidos en cariópsides (explantes) maduros cultivados en medio MS basal suplementado con 2,4-ácido diclorofenoxiacético y varias citocininas. Los medios MS+2,4-D+BAP suplementados con sorbitol (MI-13, MI-14) dieron origen a callos con características morfogénicas con potencial de regeneración. Los callos embriogénicos obtenidos a partir de MI-14 fueron colocados en diferentes medios de regeneración, entre los que MR-2 mostró la mayor frecuencia de regeneración (95.8 %) y eficiencia de conversión (13.9 %). Plántulas verdes, morfológicamente normales, fueron obtenidas con medio suplementado con cinetina (1 mg L-1), ácido naftalenacético (0.2 mg L-1) y ácido giberélico (0.2 mg L-1). El estrés osmótico y el balance hormonal resultante de la adición de sorbitol, estimuló la formación de proembroides en callos friables y de embriones somáticos en pasto Banderita. Se presenta aquí el primer protocolo de regeneración en esta especie apomíctica recalcitrante, que pueda ser útil en trabajos futuros basados en técnicas de cultivo de tejidos.

scholarly journals ΔMST and the Regulation of Cardiac CSE and OTR Expression in Trauma and Hemorrhage

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 233
Author(s):  
Britta Trautwein ◽  
Tamara Merz ◽  
Nicole Denoix ◽  
Csaba Szabo ◽  
Enrico Calzia ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Life Stress ◽  
Early Life Stress ◽  
Significant Loss ◽  
Mouse Heart ◽  
Wild Type ◽  
Complex Iv ◽  
Mercaptopyruvate Sulfurtransferase ◽  
Cellular Bioenergetics ◽  
Genetic Deletion

Genetic deletion of 3-mercaptopyruvate sulfurtransferase (MST) is known to result in hypertension and cardiac hypertrophy in older mice, and is associated with increased anxiety-like behaviors. Endogenous hydrogen sulfide (H2S) produced by MST in the mitochondria is also known to be involved in physiological and cellular bioenergetics, and its dysfunction associated with depressive behavior and increased cardiovascular morbidity. Interestingly, early life stress has been shown to lead to a significant loss of cystathionine-γ-lyase (CSE) and oxytocin receptor (OTR) expression in the heart. Thus, we were interested in testing the hypothesis of whether genetic MST mutation (ΔMST) would affect cardiac CSE and OTR expression and affect the mitochondrial respiration in a clinically relevant, resuscitated, mouse model of trauma and hemorrhagic shock. In ΔMST mice, we found a reduction of CSE and OTR in both the naive as well as injured state, in contrast to the wild type (wt) controls. Interestingly, the ΔMST showed a different complex IV response to injury than the wt controls, although our claims are based on the non-demonstrated assumption that naive wt and naive ΔMST mice have comparable complex IV activity. Finally, hemorrhagic shock led to a reduction of CSE and OTR, confirming previous results in the injured mouse heart. To date, the exact mechanisms of the cardiac interaction between H2S and OT are not clear, but they point the way to potential cardioprotective therapies.

scholarly journals COA6 is a mitochondrial complex IV assembly factor critical for biogenesis of mtDNA-encoded COX2

2015 ◽  
Vol 24 (19) ◽  
pp. 5404-5415 ◽  
Author(s):  
David A. Stroud ◽  
Megan J. Maher ◽  
Caroline Lindau ◽  
F.-Nora Vögtle ◽  
Ann E. Frazier ◽  
...  
Keyword(s):  
Mitochondrial Complex ◽  
Complex Iv ◽  
Assembly Factor

scholarly journals Early-adolescent antibiotic exposure results in mitochondrial and behavioral deficits in adult male mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Anouk C. Tengeler ◽  
Tim L. Emmerzaal ◽  
Bram Geenen ◽  
Vivienne Verweij ◽  
Miranda van Bodegom ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Mitochondrial Function ◽  
Adolescent Male ◽  
Mitochondrial Complex ◽  
Mitochondrial Translation ◽  
Behavioral Screening ◽  
Behavioral Deficits ◽  
Complex Iv ◽  
Marble Burying ◽  
Behavior And Cognition

AbstractExposure to antibiotic treatment has been associated with increased vulnerability to various psychiatric disorders. However, a research gap exists in understanding how adolescent antibiotic therapy affects behavior and cognition. Many antibiotics that target bacterial translation may also affect mitochondrial translation resulting in impaired mitochondrial function. The brain is one of the most metabolically active organs, and hence is the most vulnerable to impaired mitochondrial function. We hypothesized that exposure to antibiotics during early adolescence would directly affect brain mitochondrial function, and result in altered behavior and cognition. We administered amoxicillin, chloramphenicol, or gentamicin in the drinking water to young adolescent male wild-type mice. Next, we assayed mitochondrial oxidative phosphorylation complex activities in the cerebral cortex, performed behavioral screening and targeted mass spectrometry-based acylcarnitine profiling in the cerebral cortex. We found that mice exposed to chloramphenicol showed increased repetitive and compulsive-like behavior in the marble burying test, an accurate and sensitive assay of anxiety, concomitant with decreased mitochondrial complex IV activity. Our results suggest that only adolescent chloramphenicol exposure leads to impaired brain mitochondrial complex IV function, and could therefore be a candidate driver event for increased anxiety-like and repetitive, compulsive-like behaviors.

scholarly journals Non-additive interactions between mitochondrial complex IV blockers and hypoxia in rat carotid body responses

2014 ◽  
Vol 190 ◽  
pp. 62-69 ◽  
Author(s):  
David F. Donnelly ◽  
Insook Kim ◽  
Eileen M. Mulligan ◽  
John L. Carroll
Keyword(s):  
Carotid Body ◽  
Mitochondrial Complex ◽  
Complex Iv ◽  
Additive Interactions

scholarly journals Neuronal-specific function of hTim8a in Complex IV assembly provides insight into the molecular mechanism underlying Mohr-Tranebjærg syndrome

2019 ◽  
Author(s):  
Yilin Kang ◽  
Alexander J. Anderson ◽  
David P. De Souza ◽  
Catherine S. Palmer ◽  
Kenji M. Fujihara ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Disease ◽  
Neuronal Cells ◽  
Underlying Mechanism ◽  
Copper Chaperone ◽  
Intermembrane Space ◽  
Specific Function ◽  
Hydrophobic Membrane ◽  
Complex Iv ◽  
Enhanced Sensitivity

AbstractHuman Tim8a is a member of an intermembrane space chaperone network, known as the small TIM family, which transport hydrophobic membrane proteins through this compartment. Mutations in TIMM8A cause a neurodegenerative disease, Mohr-Tranebjærg syndrome (MTS), which is characterised by sensorineural hearing loss, dystonia and blindness. Nothing is known about the function of hTim8a in neuronal cells and consequently how lack of hTim8a leads to a neurodegenerative disease. We identified a novel cell-specific function of hTim8a in the assembly of Complex IV, which is mediated through a transient interaction with the copper chaperone COX17. Complex IV assembly defects in cells lacking hTim8a leads to oxidative stress and changes to key apoptotic regulators, including cytochrome c and Bax, which primes cells for cell death. Alleviation of oxidative stress using Vitamin E rescues cells from apoptotic vulnerability. We hypothesis that enhanced sensitivity of neuronal cells to apoptosis is the underlying mechanism of MTS.

scholarly journals Aging of Podospora anserina Leads to Alterations of OXPHOS and the Induction of Non-Mitochondrial Salvage Pathways

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3319
Author(s):  
Verena Warnsmann ◽  
Jana Meisterknecht ◽  
Ilka Wittig ◽  
Heinz D. Osiewacz
Keyword(s):  
Protein Complexes ◽  
Mitochondrial Protein ◽  
Podospora Anserina ◽  
Mitochondrial Morphology ◽  
Complex Iv ◽  
Protein Levels ◽  
Age Dependent ◽  
Functionally Impaired ◽  
Salvage Pathways

The accumulation of functionally impaired mitochondria is a key event in aging. Previous works with the fungal aging model Podospora anserina demonstrated pronounced age-dependent changes of mitochondrial morphology and ultrastructure, as well as alterations of transcript and protein levels, including individual proteins of the oxidative phosphorylation (OXPHOS). The identified protein changes do not reflect the level of the whole protein complexes as they function in-vivo. In the present study, we investigated in detail the age-dependent changes of assembled mitochondrial protein complexes, using complexome profiling. We observed pronounced age-depen-dent alterations of the OXPHOS complexes, including the loss of mitochondrial respiratory supercomplexes (mtRSCs) and a reduction in the abundance of complex I and complex IV. Additionally, we identified a switch from the standard complex IV-dependent respiration to an alternative respiration during the aging of the P. anserina wild type. Interestingly, we identified proteasome components, as well as endoplasmic reticulum (ER) proteins, for which the recruitment to mitochondria appeared to be increased in the mitochondria of older cultures. Overall, our data demonstrate pronounced age-dependent alterations of the protein complexes involved in energy transduction and suggest the induction of different non-mitochondrial salvage pathways, to counteract the age-dependent mitochondrial impairments which occur during aging.

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