Transformation of Penicillium chrysogenum using the Aspergillus nidulans amdS gene as a dominant selective marker

1987 ◽  
Vol 11 (8) ◽  
pp. 639-641 ◽  
Author(s):  
Raj K. Beri ◽  
Geoffrey Turner
1981 ◽  
Vol 1 (2) ◽  
pp. 94-100 ◽  
Author(s):  
G Charlang ◽  
B Ng ◽  
N H Horowitz ◽  
R M Horowitz

Aspergillus nidulans and Penicillium chrysogenum produce specific cellular siderophores in addition to the well-known siderophores of the culture medium. Since this was found previously in Neurospora crassa, it is probably generally true for filamentous ascomycetes. The cellular siderophore of A. nidulans is ferricrocin; that of P. chrysogenum is ferrichrome. A. nidulans also contains triacetylfusigen, a siderophore without apparent biological activity. Conidia of both species lose siderophores at high salt concentrations and become siderophore dependent. This has also been found in N. crassa, where lowering of the water activity has been shown to be the causal factor. We used an assay procedure based on this dependency to reexamine the extracellular siderophores of these species. During rapid mycelial growth, both A. nidulans and P. chrysogenum produced two highly active, unidentified siderophores which were later replaced by a less active or inactive product--coprogen in the case of P. chrysogenum and triacetylfusigen in the case of A. nidulans. N. crassa secreted coprogen only. Fungal siderophore metabolism is varied and complex.


Gene ◽  
1987 ◽  
Vol 53 (1) ◽  
pp. 63-71 ◽  
Author(s):  
Catherine M. Corrick ◽  
Andrea P. Twomey ◽  
Michael J. Hynes

1995 ◽  
Vol 246 (2) ◽  
pp. 223-227 ◽  
Author(s):  
Nathalie Bonnefoy ◽  
Jane Copsey ◽  
Michael J. Hynes ◽  
Mervl A. Davis

2003 ◽  
Vol 270 (9) ◽  
pp. 1958-1968 ◽  
Author(s):  
Francisco J. Fernandez ◽  
Rosa E. Cardoza ◽  
Eduardo Montenegro ◽  
Javier Velasco ◽  
Santiago Gutierrez ◽  
...  

Gene ◽  
1995 ◽  
Vol 160 (1) ◽  
pp. 137-138 ◽  
Author(s):  
Florentine Marx ◽  
Hubertus Haas ◽  
Sabine Hofer ◽  
Georg Stöffler ◽  
Bernhard Redl

2016 ◽  
Vol 7 ◽  
Author(s):  
Sara Domínguez ◽  
M. Belén Rubio ◽  
Rosa E. Cardoza ◽  
Santiago Gutiérrez ◽  
Carlos Nicolás ◽  
...  

1982 ◽  
Vol 150 (2) ◽  
pp. 785-787 ◽  
Author(s):  
G Charlang ◽  
R M Horowitz ◽  
P H Lowy ◽  
B Ng ◽  
S M Poling ◽  
...  

Genetics ◽  
1990 ◽  
Vol 124 (3) ◽  
pp. 585-591 ◽  
Author(s):  
G Faugeron ◽  
L Rhounim ◽  
J L Rossignol

Abstract Repeated genes, artificially introduced in Ascobolus immersus by integrative transformation, are frequently inactivated during the sexual phase. Inactivation is observed in about 50% of meioses if duplicated genes are at ectopic chromosomal locations, and in 90% of meioses if genes are tandemly repeated. Inactivation is associated with extensive methylation of the cytosine residues of the duplicated sequences and is induced in the still haploid nuclei of the dikaryotic cell which will undergo karyogamy and subsequent meiosis. Only repeated sequences become methylated. This raises the intriguing question of how the premeiotic inactivation machinery is informed that a nucleus contains multiple copies of a gene. By using in crosses recombinant strains of A. immersus in which either one, two or three genetically independent copies of the exogenous amdS gene from Aspergillus nidulans had been introduced, we could follow the premeiotic inactivation of each one of the ectopic amdS copies. This led us to propose that a prerequisite for inactivation is a premeiotic pairing of repeated sequences and that each copy can undergo successive cycles of pairing. In fact, once methylated, a copy can pair with a still unmethylated copy, so that an uneven number of copies can be subject to inactivation.


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