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Published on: March 29, 2012
Senescence in fungi: the view from Neurospora
Ramesh Maheshwari1, Arunasalam Navaraj
1Department of Biochemistry, Indian Institute of Science, Bangalore, India. fungi@biochem.iisc.ernet.in
Abstract:
Some naturally occurring strains of fungi cease growing through successive subculturing, i.e., they senesce. In Neurospora, senescing strains usually contain intramitochondrial linear or circular plasmids. An entire plasmid or its part(s) integrates into the mtDNA, causing insertional mutagenesis. The functionally defective mitochondria replicate faster than the wild-type mitochondria and spread through interconnected hyphal cells. Senescence could also be due to spontaneous lethal nuclear gene mutations arising in the multinucleated mycelium. However, their phenotypic effects remain masked until the nuclei segregate into a homokaryotic spore, and the spore germinates to form a mycelium that is incapable of extended culturing. Ultimately the growth of a fungal colony ceases due to dysfunctional oxidative phosphorylation. Results with senescing nuclear mutants or growth-impaired cytoplasmic mutants suggest that mtDNA is inherently unstable, requiring protection by as yet unidentified nuclear-gene-encoded factors for normal functioning. Interestingly, these results are in accord with the endosymbiotic theory of origin of eukaryotic cells.
Insights
Fungal senescence, or growth cessation, is linked to mitochondrial DNA instability and mutations. These genetic changes, often involving plasmids, disrupt cellular function and energy production, impacting fungal growth.
Area of Science:
- Mycology
- Cell Biology
- Genetics
Background:
- Some fungal strains exhibit senescence, ceasing growth during subculturing.
- Senescence in Neurospora is often associated with intramitochondrial plasmids integrating into mitochondrial DNA (mtDNA).
- This integration causes insertional mutagenesis, leading to defective mitochondria.
Purpose of the Study:
- To investigate the mechanisms underlying fungal senescence.
- To explore the role of mitochondrial DNA instability and nuclear gene mutations in senescence.
- To understand the implications for fungal growth and cellular function.
Main Methods:
- Analysis of senescing fungal strains, including Neurospora.
- Examination of intramitochondrial plasmids and their integration into mtDNA.
- Study of nuclear gene mutations and their phenotypic effects.
- Investigation of mitochondrial replication and spread in interconnected hyphae.
Main Results:
- Senescing strains frequently harbor plasmids that integrate into mtDNA, causing mutations.
- Defective mitochondria replicate faster and spread, leading to impaired oxidative phosphorylation.
- Nuclear gene mutations can also cause senescence, with effects masked until spore germination.
- mtDNA appears inherently unstable, requiring nuclear-encoded factors for stability.
Conclusions:
- Fungal senescence results from mtDNA instability or nuclear mutations affecting mitochondrial function.
- Dysfunctional mitochondria and impaired oxidative phosphorylation ultimately halt colony growth.
- The findings support the endosymbiotic theory of eukaryotic cell origins.
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