β-Alanine transaminase activity in black and suppressor of black mutations of Drosophila melanogaster

A Member of the p38 Mitogen-Activated Protein Kinase Family Is Responsible for Transcriptional Induction ofDopa decarboxylasein the Epidermis ofDrosophila melanogasterduring the Innate Immune Response

“…Presumably, DA is metabolized by the enzymes responsible for the production of sclerotin since no melanin deposits are evident within the epidermis. Consistent with this prediction, the gene black, whose protein product is an enzyme involved in NBAD synthesis (30,62,82), is also upregulated in the Drosophila immune response (34). Future research will reveal the extent of the antimicrobial role of quinone production in the innate immune response.…”

Catecholamine metabolism and in vitro induction of premature cuticle melanization in wild type and pigmentation mutants ofDrosophila melanogaster

“…Mutations in a third gene known to affect cuticle pigmentation is black. It has recently been proposed that b mutations increase the level of J3-alanine transaminase, thus stimulating p-alanine catabolism (Weber et al, 1992). Consequently, mutations in b result in reduced levels of p-alanine (Hodgetts, 1972;Hodgetts and Choi, 1974;Sherald, 1981;Black, unpublished data).…”

Analysis of Pyrimidine Catabolism inDrosophila melanogasterUsing Epistatic Interactions With Mutations of Pyrimidine Biosynthesis and β-Alanine Metabolism

“…Uracil catabolism is the major source of b-alanine in flies (Ross and Monroe 1972) in which adult cuticle pigmentation is qualitatively dependent upon b-alanine levels in cuticle-forming cells (Wright 1987). For example, black (b) mutant animals display a uniformly black cuticle phenotype, low levels of b-alanine (Hodgetts 1972), and an abnormal increase in the catabolic enzyme balanine transaminase (Weber et al 1992). The b phenotype is reversed by injection of uracil, dihydrouracil, ureidopropionate, or b-alanine (Hodgetts and Choi 1974;Jacobs 1974).…”