A translocation activating the cryptic nitrogen regulation gene areB inactivates a previously unidentified gene involved in glycerol utilisation in Aspergillus nidulans

Abstract

The chromosome VIII translocation breakpoint of the areB-404 translocation, selected for its ability to activate the cryptic nitrogen metabolism regulatory gene areB, and the mutation glcD-100 both lead to loss of mitochondrial FAD-dependent sn-glycerol-3-phosphate dehydrogenase in Aspergillus nidulans. These two lesions therefore define glcD, a second gene (in addition to glcB) where mutation can result in loss of this enzyme. The glcD gene has been localised to a centromere-proximal region of the right arm of chromosome VIII. Although all six known areB-activating mutations involve chromosomal rearrangements and presumably therefore gene fusions, areB-404 is the first such rearrangement where the gene involved in an areB fusion has been identified.

The Validity of theAspergillus nidulansLinkage Map

“…The general arrangement of this chromosome has been securely determined by mitotic mapping using chaA and fwA as visually selectable spore color markers (Wood and Käfer, 1967;Käfer, 1976), T2(I;VIII)-sD50 (Ma and Käfer, 1974), niaD selected by virtue of chlorate resistance (Arst et al, 1990), and ureA selected for thiourea resistance (K. Sharma, H. M. Sealy-Lewis, and C. Scazzocchio, unpublished). Clutterbuck (1970) also analyzed partial disomics for VIIIR segregating from crosses involving the nonreciprocal T2(III;VIII)-brlA12.…”

Glycerol catabolism in Aspergillus nidulans

“…Since all other enzyme levels in this mutant are comparable to those of the wild-type on each of the carbon sources tested (data not shown), it is probable that the glcGl mutant, like the glcB33 mutant, is defective in the mitochondrial G3P dehydrogenase activity. In the glcDI00 mutant FAD-dependent G3P dehydrogenase activities are also greatly decreased (Arst et al, 1990). The glcD100 mutation was found to be located on chromosome VIII (Arst et al, 1990).…”

“…nidulans. glcA mutations were proposed to lead to glycerol kinase deficiency, glcB and glcD strains are deficient for the mitochondrial glycerol-3-phosphate dehydrogenase (Payton, 1978 ;Uitzetter, 1982;Arst et al, 1990) and glcC strains are defective in glycerol uptake (Visser et al, 1988) A . nidulans is therefore likely to use the phosphorylating pathway.…”

Deletion and overexpression of the Aspergillus nidulans GATA factor AreB reveals unexpected pleiotropy

“…The areB gene was first identified by mutations involving chromosomal rearrangement at the areB locus that suppressed an areA null mutant (Tollervey & Arst, 1982;Arst et al, 1989Arst et al, , 1990. It was proposed that these gain-of-function areB mutations were due to fusion of a cryptic activation domain to the GATA DNA-binding region of AreB (Conlon et al, 2001).…”