BLACK
-Although the microinjection experiments showed that
The gene black is referred to in FlyBase by the symbol
Dmel\b (CG7811, FBgn0000153). It is a the pupal case, it appears that this mutant simply does
SO0000010:protein_coding_gene from Drosophila
melanogaster. It has 3 annotated transcripts and 3
polypeptides (2 unique). Gene sequence location is
2L:13821248..13823979. It has the cytological map location
34D1. Protein features are: Pyridoxal phosphate-
dependent decarboxylase; Pyridoxal phosphate-
dependent transferase; Pyridoxal phosphate-dependent
transferase, major domain. Its molecular function is
described by: aspartate 1-decarboxylase activity;
pyridoxal phosphate binding. It is involved in the
biological process described with: visual behavior; uracil
catabolic process; developmental pigmentation;
carboxylic acid metabolic process; beta-alanine
biosynthetic process. 220 alleles are reported. The
phenotypes of these alleles manifest in: wing vein; adult
cuticle; puparium cuticle; tarsal segment; trident. The
phenotypic classes of alleles include: body color
defective; viable; lethal; pain response defective; visible;
visual behavior defective. Summary of modENCODE
Temporal Expression Profile: Temporal profile ranges
from a peak of very high expression to a trough of very
low expression. Peak expression observed at stages
throughout the pupal period.
b: black (M. Ashburner)
Black pigment on body and tarsi and along wing veins.
Reflectance of cuticle 40% that of wild type (Pedersen,
1982, Carlsberg Res. Comm. 47: 391-400). Heterozygote
somewhat darker than wild type, especially on trident,
but never confused with homozygote. Body color darker
at low temperature (Sherald, 1981, Mol. Gen. Genet. 183:
102-06). Puparium lighter than wild type. Not easily
classified in newly emerged flies (Waddington, 1941, Proc.
Zool. Soc. London Ser. A. 111: 173-80). Tyrosinase
formed in adult flies (Horowitz). Fails to synthesize beta-
alanine (Hodgetts, 1972, J. Insect Physiol. 18: 937-47), and
feeding or injection of beta-alanine to b produces normal
phenotype [Jacobs, 1974, J. Insect Physiol. 20: 859-66;
Hodgetts, Hodgetts and Choi, 1974, Nature (London) 252:
710-11]. Also corrected by feeding 6-azauracil (Pedersen,
1982, Hereditas 97: 329); feeding 6-azathymine produces
weak b phenocopy which is suppressed by Su(b)
(Pedersen). ERG normal [Hotta and Benzer, 1969, Nature
(London) 22: 354-56]. Puparial case structurally abnormal
with wide, diffuse, exocuticular lamellae and indistinct
endocuticular fibrils (Jacobs, 1978, Insect Biochem. 8: 37-
41). Pupae UV sensitive (Jacobs 1978). Suppressed by
su(b) (Sherald, 1981, Mol. Genet. 181: 102-106) and Su(b)
(Pedersen); enhanced by sp2 (Gubb) and su(r) (Pedersen).
su(r) su(b) b is enhanced black; su(r) b not enhanced by
feeding 6-azauracil (Pedersen). Possibly structural gene for
beta-ureidopropionase (EC 3.5.1.6; Sherald). RK1 in aged
flies.
B-alanine pathways
Pyrimidine metabolism
Pantothenate and CoA biosynthesis
Biosynthesis of secondary metabolites
Neuroactive ligand-receptor interaction
Protein digestion and absorption
black is capable of incorporating injected b-alanine into
not manufacture a sufficient quantity of the amino acid in
the period between puparium formation and the larval-
pupal apolysis to cause normal tanning (HODGETTS,
1973).
-Two mutants, ebony and black, which fail to tan the
pupal case were shown to be defective in the metabolism
of b-alanine. Pharate pupae of ebony are able to
manufacture the compound but unable to utilize it.
Pharate pupae of black are unable to manufacture the
substance, but can utilize b-alanine if it is supplied to
them during the larval stage (HODGETTS, 1973).
-The sclerotisation and tanning of insect cuticles is
generally thought to result from a crosslinking of
cuticular proteins by quinonoid derivatives of tyrosine. B-
alanine is a constituent of the cuticles of many insects,
and it is required for normal tanning of pupal case of
several insects. In D. melanogaster failure to utilize the
compound result in an untanned pupal case, where as in
Musca domestica, Bombyx mori and D. virillis failure to
incorporate b-alanine result in abnormally black cases.
-Recently we reported that substantial amounts of
dopamine accumulate prior to eclosion in D.
melanogaster. Oxidation of this dopamine to indole-5,6-
quinone would be expected when O2 becomes available
after eclosion, and melanisation would ensue if the
indole-5,6-quinone molecules polymerized. Because
melanin deposition over a large part of the adult cuticle
of D. melanogaster does not normally occur, we
postulated that extensive polymerization was prevented
by b-alanine. On this basis, the extensive polymerization
was prevented by B-alanine.
- The pupa cases of black are also less compact than
normal (Jacobs 1978), thus implicating b-alanine as a
participant in sclerotization (hardening) of the cuticle as
well as in coloration.
- Adult melanization is inversely related to the rate of
incorporation of beta-alanine into tanning cuticles.
-N-acetyldopamine is derived by the following pathway:
tyrosine~dopa~dopamine~N-acetyldopamine. It passes
into the cuticle to meet the oxidase, which oxidizes it to
the tanning quinone. This oxidation proceeds rapidly if
the highly reactive quinone finds a complexing site.b-
Alanine provides such a site, and, reacting quickly,
produces an orange-red complex which leads to tanning
of' the cuticle. In the absence of b-alanine, precursors in
the pathway may accumulate because of feedback
inhibition. A gradation between extremes of tanning and
blackening may exist in various insects, depending on the
relative concentration of/?-alanine and dopamine
available. Abundant dopamine may lead to melanization,
obscuring an underlying/3-alanine plus quinone tanning
(Jacobs, 1980)