Strain: Neurospora crassa

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FGSC #1689

Mutant Type

Genus: N

reporting_genes: ssu-2;am;al

species: Neurospora crassa

allele: WRU35;am17;no#

stock: am17 RU35

glasgow:

mutagen: UV

Depositor: TWS

Link Group: IR;VR;--

MT: A

Species No: 10

gene_back:

oppmt: 0

trans:

ref1: Seale 1968. Genetics 58:85-99, https://www.genetics.org/content/genetics/58/1/85.full.pdf;

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-1689

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-1689 ↗

Genes

Locus Cultural Requirements Link Group Type
amVR. Right of ure-2 (2%) and sp (4 to 8%). Left of gul-1(<<1%) and ace-5(<1%) (122, 570, 579, 998). (R.W. Barratt, (cited in reference 1036) Structural gene for nicotinamide adenine dinucleotide phosphate (NADP)-glutamate dehydrogenase (336) (see Fig. 19), for which a complete 452-residue amino acid sequence has been obtained (465). Requires a source of alpha-amino nitrogen for growth, alanine being a good supplement (e.g., reference 997). Readily scorable at 25 C; leaky at 34°C (42). Leaky growth and adaptation on minimal medium are prevented by 0.02 M glycine (782, 783) or by en(am)-1, en(am)-2, or nit-2, q.v. The ammutants show abnormal regulation of reduced nicotinamide adenine dinucleotide (NADH)-glutamate dehydrogenase and are synergistic with nit-2 in this effect (226). Some am alleles (e.g., RU1) suppress the pyrimidine requirement caused by pyr-3 (CPS- ACT+) mutations (1137). Used for the first demonstration of complementation between alleles in vivo (344) (simultaneous with independent demonstration with ad-4). In vitro complementation (342). Used for studies of complementation mechanism (199, 200, 1120). Used for fine-structure mapping (337, 338). Control of intralocus recombination by rec-3(996-998). Used to study colinearity of the gene and gene product, internal suppressors (105, 340, 465), and the action of supersuppressors (954, 955). The functional defects in several mutant enzymes with single amino acid replacements have been defined: am1 mutant enzymes fail to bind NADPH (1120); am2, am3, am19, am130, and am131 enzymes are stabilized in the inactive conformational form (30, 200, 336, 556, 1044), and all are complementable by am1; am14 is osmotically reparable and is thought to have unstable quaternary structure (340). Used in a study showing glutamine to have a role as corepressor of uricase synthesis (1118). Used to study nitrogen assimilation and metabolism (503) and nitrogen metabolite repression (186, 291). Efficient procedure for selecting new am mutants (551). Spectrum of ultraviolet irradiation (UV)- and nitrous acid-induced mutants (554). Allele am17 has a chain-terminating codon of either the amber or ochre type at residue 313 of glutamate dehydrogenase, based on amino acid replacements in revertants and by ssu-1 (956). Allele 6 is a frameshift mutation with an insertion in the Ser5 codon (985). Allele 126 is highly unstable (553). Allele 132 is a deletion (1162). The am+ gene has been cloned in Escherichia coli(J.R.S. Fincham, personal communication) and transformed back into Neurospora (J.A. Kinsey, personal communication).VRB
ssu-2I. Linked to mt (22%), probably between the centromere (7%) and al-2(26%). Recombines with ssu-3 (954). Allele WRU35 selected (954) as a coincident suppressor of nonsense mutations trp-3 (td140) and am(17), which may be either amber or ochre but cannot be UGA (956). Also suppresses certain nonsense alleles of trp-1, trp-2, and ad-3B(see reference 955).IB
alMutants designated as albino impair carotenoid synthesis. These affect only vegetative cells (mycelia and conidia) and are without known effect on the perithecia or ascospores, where the pigment is melanin. The albino mutants vary in amount and color of carotenoids. Different alleles result in conidia and mycelia that are white, yellow, pink, purple, or white with traces of color or in white mycelia with pigment in the peripheral conidia. See, for example, reference 1042. Carotenoid synthesis is also affected by ylo, wc, and age-3, q.v., and by modifiers of intensity (982). Albino mutants have been used to study the role of carotenoids in photoprotection (984, 1071, and references therein). Rapid development of carotenoids is induced by light; the action spectrum is described in references 250 and 1181, and mechanism of photocontrol is considered in reference 444. However, carotenoid synthesis can proceed slowly in complete darkness. Maximum carotenoid production results if incubation is at 6°C immediately after exposure to inducing light (442). Albino mutants can be scored in submerged colonies from plated ascospores by transfer of sorbose plates to 4 C under light after colonies have grown at 25°C in the dark (154, 500). An unstable constitutive variant has been described (587). Most al mutations map in a short region of IR where al-1 and al-2 were previously thought to be contiguous but are now known to be separated by other loci (797; D.D. Perkins, unpublished data).B

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