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Suppression of kalDNA-related senescence in Neurospora Yang, Xiao
Abstract
Senescence in Neurospora, the progressive loss of growth potential culminating in death, is caused by the insertion of a linear mitochondrial plasmid kalDNA into the mitochondrial chromosomes. Investigation of the suppression of kalDNA-related senescence in Neurospora has revealed that there are three mechanisms of suppressing the kalDNA- related senescence in Neurospora. The first mechanism is that one allele of one nuclear gene from strain 83 inhibits the replication of the kalilo plasmid to a very low level in the mitochondria, there are no (or too few) IS-kalDNAs to affect the normal function of the mitochondria. The other allele of the gene from strain HB9006 permits the.plasmid to replicate to high levels, thus the insertion activities of the plasmid destroy the mitochondrial function and consequently cause death of the host fungus. The second mechanism is the cytoplasmic segregation. The mitochondria in senescent strains are heterogenic, some containing AR-kalDNA or and IS-kalDNAs, some containing neither. When asci, ascospores or conidia are formed with the mitochondria lacking kalDNA from their parental cytoplasm containing kalDNA, the sexual or asexual progeny with normal mitochondria grow immortally, escaping the fate of death. The third mechanism is that of a nuclear gene with two alleles in ascus 13. One allele of this gene from HB9006 cannot suppress the deleterious function of IS-kalDNAs, resulting in vegetative death. The other allele of this gene, from strain 428, allows the plasmid to replicate normally and insert into the mitochondrial chromosomes generating IS-kalDNAs, but the allele somehow suppresses the deleterious effects of IS-kalDNAs, resulting in the host fungi growing normally, and carrying both AR-kalDNA and IS-kalDNAs in their mitochondria. The kinetic studies of mitochondrial kalDNA in senescent Neurospora strains have revealed the general trend of kalDNA changes in the kalilo senescence process. The free form (AR- kalDNA) of the plasmid is observed in all subcultures of senescent series, increases in quantity at the early stage of senescence until a peak is reached at the late stage, and then drops to a low level. The inserted form (IS-kalDNA) of the plasmid is not observed at the early stage, but observed at the late stage and increases in quantity until the last analyzable subcultures. The relationship of AR-kalDNA and IS-kalDNA, and their replication characteristics have been discussed. A model of accumulation of IS-kalDNA has been proposed.
Item Metadata
Title |
Suppression of kalDNA-related senescence in Neurospora
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Creator | |
Publisher |
University of British Columbia
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Date Issued |
1991
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Description |
Senescence in Neurospora, the progressive loss of growth potential culminating in death, is caused by the insertion of a linear mitochondrial plasmid kalDNA into the mitochondrial chromosomes. Investigation of the suppression of kalDNA-related senescence in Neurospora has revealed that there are three mechanisms of suppressing the kalDNA-
related senescence in Neurospora. The first mechanism is that one allele of one nuclear
gene from strain 83 inhibits the replication of the kalilo plasmid to a very low level in the mitochondria, there are no (or too few) IS-kalDNAs to affect the normal function of the mitochondria. The other allele of the gene from strain HB9006 permits the.plasmid to replicate to high levels, thus the insertion activities of the plasmid destroy the mitochondrial function and consequently cause death of the host fungus. The second mechanism is the cytoplasmic segregation. The mitochondria in senescent strains are heterogenic, some containing AR-kalDNA or and IS-kalDNAs, some containing neither. When asci, ascospores or conidia are formed with the mitochondria lacking kalDNA from their parental cytoplasm containing kalDNA, the sexual or asexual progeny with normal mitochondria grow immortally, escaping the fate of death. The third mechanism is that of a nuclear gene with two alleles in ascus 13. One allele of this gene from HB9006 cannot suppress the deleterious function of IS-kalDNAs, resulting in vegetative death. The other allele of this gene, from strain 428, allows the plasmid to replicate normally and insert into the mitochondrial chromosomes generating IS-kalDNAs, but the allele somehow suppresses the deleterious effects of IS-kalDNAs, resulting in the host fungi growing normally, and carrying both AR-kalDNA and IS-kalDNAs in their mitochondria.
The kinetic studies of mitochondrial kalDNA in senescent Neurospora strains have revealed the general trend of kalDNA changes in the kalilo senescence process. The free form (AR-
kalDNA) of the plasmid is observed in all subcultures of senescent series, increases in quantity at the early stage of senescence until a peak is reached at the late stage, and then drops to a low level. The inserted form (IS-kalDNA) of the plasmid is not observed at the early stage, but observed at the late stage and increases in quantity until the last analyzable subcultures. The relationship of AR-kalDNA and IS-kalDNA, and their replication characteristics have been discussed. A model of accumulation of IS-kalDNA has been proposed.
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Genre | |
Type | |
Language |
eng
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Date Available |
2010-11-05
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Provider |
Vancouver : University of British Columbia Library
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Rights |
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
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DOI |
10.14288/1.0098528
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URI | |
Degree | |
Program | |
Affiliation | |
Degree Grantor |
University of British Columbia
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Campus | |
Scholarly Level |
Graduate
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Aggregated Source Repository |
DSpace
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For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.