کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10939723 | 1095323 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Intramolecular recombination and deletions in mitochondrial DNA of senescent, a nuclear-gene mutant of Neurospora crassa exhibiting “death” phenotype
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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چکیده انگلیسی
In Neurospora crassa, a nuclear-gene mutant, senescent, derived from a phenotypically normal wild isolate of Neurospora intermedia exhibits a 'death' phenotype. Regardless of the composition of the culture medium, the mycelium ceases to grow in 2-6 subcultures at 26 °C and 1 or 2 subcultures at 34 °C. Senescence of vegetative mycelium is associated with deficiencies in cytochromes aa3 and b and reduced oxygen uptake. The restriction fragment analysis of mitochondrial DNA from senescing mycelia showed deletions and gross sequence rearrangements. Analysis of mitochondrial DNA of (sen + sen+) heterokaryons constructed with “excess” sen cytoplasm suggested correlation between mtDNA deletions and senescence. Three novel sen-specific EcoRI fragments of sizes 3.6, 3.9, and 4.4 kb were cloned, sequenced, and analyzed. Nucleotide sequences of the sen-specific EcoRI fragments suggested that deletions were a consequence of intramolecular recombination between EcoRI-5 and -10 and/or between EcoRI-8 and -10. The recombination junctions were close to stretches of GC-rich-PstI palindromic sequences that potentially form stable hairpin structures and might facilitate recombination between homologous repeats as short as 6-10 bp. These observations suggest that the wild-type (sen+) allele encodes a factor that protects the mitochondrial genome from undergoing intramolecular recombination and deletions. In this respect sen+ (linkage group V) has a function similar to nd+ (linkage group I) and the two gene products probably have mutually exclusive roles in suppressing cruciform-associated and homologous recombination, respectively, thus safeguarding mitochondrial genome integrity. The sen+ allele most likely codes for a factor involved in recombination, repair or replication of the mitochondrial genome, or a transcription factor that regulates the expression of genes affiliated with mitochondrial DNA metabolism.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Fungal Genetics and Biology - Volume 42, Issue 2, February 2005, Pages 178-190
Journal: Fungal Genetics and Biology - Volume 42, Issue 2, February 2005, Pages 178-190
نویسندگان
Anthony D. D'Souza, Helmut Bertrand, Ramesh Maheshwari,