Mitochondrial DNA integrity changes with age but does not correlate with learning performance in honey bees

2014 ◽  
Vol 49 ◽  
pp. 12-18 ◽  
Author(s):  
E.M. Hystad ◽  
G.V. Amdam ◽  
L. Eide
2021 ◽  
pp. 117720
Author(s):  
Nicole S. DesJardins ◽  
Adrian Fisher ◽  
Cahit Ozturk ◽  
Jennifer H. Fewell ◽  
Gloria DeGrandi-Hoffman ◽  
...  

2018 ◽  
Vol 62 (2) ◽  
pp. 223-232
Author(s):  
Dylan Cleary ◽  
Allen L. Szalanski ◽  
Clinton Trammel ◽  
Mary-Kate Williams ◽  
Amber Tripodi ◽  
...  

Abstract A study was conducted on the mitochondrial DNA genetic diversity of feral colonies and swarms of Apis mellifera from ten counties in Utah by sequencing the intergenic region of the cytochrome oxidase (COI-COII) gene region. A total of 20 haplotypes were found from 174 honey bee colony samples collected from 2008 to 2017. Samples belonged to the A (African) (48%); C (Eastern Europe) (43%); M (Western Europe) (4%); and O (Oriental) lineages (5%). Ten African A lineage haplotypes were observed with two unique to Utah among A lineage haplotypes recorded in the US. Haplotypes belonging to the A lineage were observed from six Utah counties located in the southern portion of the State, from elevations as high as 1357 m. All five C lineage haplotypes that were found have been observed from queen breeders in the US. Three haplotypes of the M lineage (n=7) and two of the O lineage (n=9) were also observed. This study provides evidence that honey bees of African descent are both common and diverse in wild populations of honey bees in southern Utah. The high levels of genetic diversity of A lineage honey bee colonies in Utah provide evidence that the lineage may have been established in Utah before the introduction of A lineage honey bees from Brazil to Texas in 1990.


2021 ◽  
Author(s):  
Joanna L Fiddler ◽  
Yuwen Xiu ◽  
Jamie E Blum ◽  
Simon G Lamarre ◽  
Whitney N Phinney ◽  
...  

Background. Adequate cellular thymidylate (dTMP) pools are essential for preservation of nuclear and mitochondrial genome stability. Previous studies have indicated that disruption in dTMP synthesis in the nucleus leads to increased uracil misincorporation into DNA affecting genome stability. To date, the effects of impaired mitochondrial dTMP synthesis in non-transformed tissues have been understudied. Objective. This study aimed to determine the effects of decreased serine hydroxymethyltransferase 2 (Shmt2) expression and dietary folate deficiency on mitochondrial DNA integrity and mitochondrial function in mouse tissues. Methods. Liver mitochondrial DNA (mtDNA) content, and uracil content in liver mtDNA was measured in Shmt2+/- and Shmt2+/+ mice weaned onto either a folate-sufficient control diet (2 mg/kg folic acid, C) or a modified diet lacking folic acid (0 mg/kg folic acid, FD) for 7 wks. Shmt2+/- and Shmt2+/+ mouse embryonic fibroblasts (MEF cells) were cultured in defined culture medium containing either 0 or 25 nM folate to assess proliferative capacity and mitochondrial function. Results. Shmt2+/- mice exhibited 48-67% reduction in SHMT2 protein levels in tissues. Interestingly, Shmt2+/- mice consuming the folate-sufficient C diet exhibited a 25% reduction in total folate in liver mitochondria. There was also a >20-fold increase in uracil in liver mtDNA in Shmt2+/- mice consuming the C diet, and dietary folate deficiency also increased uracil content in mouse liver mtDNA from both Shmt2+/+ and Shmt2+/- mice. Furthermore, decreased Shmt2 expression in MEF cells reduced cell proliferation, mitochondrial membrane potential, and oxygen consumption rate. Conclusions. This study demonstrates that Shmt2 heterozygosity and dietary folate deficiency impair mitochondrial dTMP synthesis, as evidenced by the increased uracil in mtDNA. In addition, Shmt2 heterozygosity impairs mitochondrial function in MEF cells. These findings suggest that elevated uracil in mtDNA may impair mitochondrial function.


2019 ◽  
Vol 20 (17) ◽  
pp. 4311 ◽  
Author(s):  
Arun Kumar Kondadi ◽  
Ruchika Anand ◽  
Andreas S. Reichert

Mitochondria are vital cellular organelles involved in a plethora of cellular processes such as energy conversion, calcium homeostasis, heme biogenesis, regulation of apoptosis and ROS reactive oxygen species (ROS) production. Although they are frequently depicted as static bean-shaped structures, our view has markedly changed over the past few decades as many studies have revealed a remarkable dynamicity of mitochondrial shapes and sizes both at the cellular and intra-mitochondrial levels. Aberrant changes in mitochondrial dynamics and cristae structure are associated with ageing and numerous human diseases (e.g., cancer, diabetes, various neurodegenerative diseases, types of neuro- and myopathies). Another unique feature of mitochondria is that they harbor their own genome, the mitochondrial DNA (mtDNA). MtDNA exists in several hundreds to thousands of copies per cell and is arranged and packaged in the mitochondrial matrix in structures termed mt-nucleoids. Many human diseases are mechanistically linked to mitochondrial dysfunction and alteration of the number and/or the integrity of mtDNA. In particular, several recent studies identified remarkable and partly unexpected links between mitochondrial structure, fusion and fission dynamics, and mtDNA. In this review, we will provide an overview about these recent insights and aim to clarify how mitochondrial dynamics, cristae ultrastructure and mtDNA structure influence each other and determine mitochondrial functions.


Aging Cell ◽  
2012 ◽  
Vol 11 (3) ◽  
pp. 456-466 ◽  
Author(s):  
Deborah L. Croteau ◽  
Marie L. Rossi ◽  
Chandrika Canugovi ◽  
Jane Tian ◽  
Peter Sykora ◽  
...  

2009 ◽  
Vol 47 (9-10) ◽  
pp. 717-721 ◽  
Author(s):  
Fulya Özdil ◽  
Bahman Fakhri ◽  
Hasan Meydan ◽  
Mehmet Ali Yıldız ◽  
H. Glenn Hall

DNA Repair ◽  
2006 ◽  
Vol 5 (1) ◽  
pp. 71-79 ◽  
Author(s):  
Alexis B. Hansen ◽  
Nicholas B. Griner ◽  
Jon P. Anderson ◽  
Greg C. Kujoth ◽  
Tomas A. Prolla ◽  
...  

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