On transition bias in mitochondrial genes of pocket gophers

1996 ◽  
Vol 43 (1) ◽  
pp. 32-40 ◽  
Author(s):  
Xuhua Xia ◽  
Mark S. Hafner ◽  
Philip D. Sudman

2009 ◽  
Vol 90 (3) ◽  
pp. 537-547 ◽  
Author(s):  
Ryan R. Chambers ◽  
Philip D. Sudman ◽  
Robert D. Bradley


2018 ◽  
Author(s):  
Maria Dafne Cardamone ◽  
Bogdan Tanasa ◽  
Carly Cedarquist ◽  
Jiawen Huang ◽  
Kiana Mahdaviani ◽  
...  


1999 ◽  
Vol 14 (3) ◽  
pp. 164-168 ◽  
Author(s):  
Michael J. Pipas ◽  
Gary W. Witmer

Abstract A 2 yr study on the Rogue River and Mt. Hood National Forests in Oregon evaluated physical barriers for protection of Pinus ponderosa seedlings against damage by Thomomys talpoides. Seedlings protected with one of three weights of: (1) plastic mesh tubing (Vexar®) or (2) sandpapertubing (Durite®) were evaluated against control seedlings. On the Rogue River sites, Vexar® seedlings had the highest survival (62.6%), followed by the controls (59.1%), then Durite® seedlings (17.9%). Gophers were the primary cause of death for the Vexar® seedlings, versus desiccation for the Durite® seedlings. On the Mt. Hood sites, heavyweight Vexar® seedlings had the highest survival (35.4%), medium-weight Durite® seedlings the lowest (2.7%). Seedling mortality caused by gophers was highest for controls (70.2%), followed by light-weight (62.2%) and heavy-weight (53.9%) Vexar® treatments. Overall survival was low (Rogue River = 42%, Mt. Hood = 19.8%). Growth was greatest for the control seedlings but only significantly greater than growth of Durite® seedlings on the Rogue River sites. Growth of seedlings was not compromised by the Vexar® tubing. Although neither type of tubing was highly protective, Vexar® tubes performed better than Durite® tubes. West. J. Appl. For. 14(3):164-168.



2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Vaibhav S. Marde ◽  
Prerna L. Tiwari ◽  
Nitu L. Wankhede ◽  
Brijesh G. Taksande ◽  
Aman B. Upaganlawar ◽  
...  

Abstract Background Over the last decade, aggregating evidences suggested that there is a causative link between mutation in gene associated with mitochondrial dysfunction and development of several neurodegenerative disorders. Main text Recent structural and functional studies associated with mitochondrial genes have shown that mitochondrial abnormalities possibly lead to mitochondrial dysfunction. Several studies on animal models of neurodegenerative diseases and mitochondrial genes have provided compelling evidence that mitochondria is involved in the initiation as well as progression of diseases such as Parkinson’s disease (PD), Alzheimer’s disease (AD), Huntington’s disease (HD), and Friedreich ataxia (FA). Conclusion In this mini-review, we have discussed the different etiologic and pathogenesis connected with the mitochondrial dysfunction and relevant neurodegenerative diseases that underlie the dominant part of mitochondrial genes in the disease development and its progress.



Genetics ◽  
2001 ◽  
Vol 157 (4) ◽  
pp. 1711-1721
Author(s):  
Donald L Auger ◽  
Kathleen J Newton ◽  
James A Birchler

Abstract Each mitochondrion possesses a genome that encodes some of its own components. The nucleus encodes most of the mitochondrial proteins, including the polymerases and factors that regulate the expression of mitochondrial genes. Little is known about the number or location of these nuclear factors. B-A translocations were used to create dosage series for 14 different chromosome arms in maize plants with normal cytoplasm. The presence of one or more regulatory factors on a chromosome arm was indicated when variation of its dosage resulted in the alteration in the amount of a mitochondrial transcript. We used quantitative Northern analysis to assay the transcript levels of three mitochondrially encoded components of the cytochrome c oxidase complex (cox1, cox2, and cox3). Data for a nuclearly encoded component (cox5b) and for two mitochondrial genes that are unrelated to cytochrome c oxidase, ATP synthase α-subunit and 18S rRNA, were also determined. Two tissues, embryo and endosperm, were compared and most effects were found to be tissue specific. Significantly, the array of dosage effects upon mitochondrial genes was similar to what had been previously found for nuclear genes. These results support the concept that although mitochondrial genes are prokaryotic in origin, their regulation has been extensively integrated into the eukaryotic cell.







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