A reddish-brown mutant in the desert locust, Schistocerca gregaria

Abstract

A reddish-brown (RB) mutant of the desert locust, Schistocerca gregaria and its genetic control are described. Hatchlings with reddish-brown patterns (RB strain) were found among normal individuals with black patterns (normal strain) in a laboratory colony. The color patterns were similar in the two strains, but the intensity of the melanization appeared weaker in the former. Hatchlings of this mutant could be distinguished visually from normal individuals under crowded conditions only, because they all became green without developing dark patterns under isolated conditions. Under crowded conditions, the difference in the darkness of the body coloration diminished as nymphs grew bigger but persisted throughout their life, including the adult stage. Reciprocal crosses between the mutant and normal strains under crowded conditions produced normal phenotypes only, indicating that the RB phenotype was recessive to the normal phenotype. In the F 2 generation, the normal and RB phenotypes appeared in a ratio of 3 : 1, indicating that the RB phenotype is inherited in a simple Mendelian fashion and the RB gene is autosomal. These results suggest that the expression of the RB phenotype is phase-dependent and the RB gene might regulate the intensity of melanization.

Genetic and hormonal control of melanization in reddish-brown and albino mutants in the desert locustSchistocerca gregaria

“…However, the present results are based on visual colours, and little is known about the pigments involved. The reddish–brown colour may not be caused simply by a reduced intensity of black pigmentation, although both reddish–brown and black pigments stain the exuviae, indicating that they are most likely melanins (Maeno & Tanaka, 2008b). The possibility that injection of [His 7 ]‐corazonin or implantation of extra CC simply masks the reddish–brown colour by inducing black pigment in the cuticle cannot be ruled out.…”

“…The normal strain of S. gregaria used has been described previously (Tanaka & Yagi, 1997; Maeno & Tanaka, 2004) and the albino strain originated from the same laboratory line as described previously (Hunter‐Jones, 1957; Schoofs et al , 2000; Yerushalmi et al , 2000b). The RB mutant was established in 2006 from reddish–brown nymphs that were found in the normal strain maintained for more than 40 generations in the Tsukuba laboratory (Maeno & Tanaka, 2008b). Nymphs and adults were kept in groups of approximately 100 individuals in large cages (42 × 22 × 42 cm) under an LD 16 : 8 h photoperiod and 50–70% relative humidity at 32 ± 1 °C, as described previously (Maeno et al , 2004).…”

“…Crossing was made according to the method of Maeno & Tanaka (2008b). Briefly, newly‐emerged female adults of each strain were separated from males and reared in a group of approximately 30 individuals for crossing.…”

“…In S. gregaria , there is an albino strain known as a pigmentation mutant (Hunter‐Jones, 1957). Recently, another type of pigmentation mutant, the reddish–brown (RB) strain, has been established (Maeno & Tanaka, 2008b). Whereas albino nymphs do not develop dark pigmentation and become whitish under crowded conditions, RB mutants develop blackish patterns similar to normal individuals, although the intensity of the melanization is weaker than that of the latter, particularly during the early stage of nymphal development.…”

“…Whereas albino nymphs do not develop dark pigmentation and become whitish under crowded conditions, RB mutants develop blackish patterns similar to normal individuals, although the intensity of the melanization is weaker than that of the latter, particularly during the early stage of nymphal development. The albino and RB phenotypes are recessive to the normal pigmented phenotype and controlled by single Mendelian unit (Hunter‐Jones, 1957; Maeno & Tanaka, 2008b). Other types of body colour mutants of S. gregaria (Volkonsky, 1938; Yerushalmi et al , 2000a) and albino strains of L. migratoria (Nolte, 1971; Hasegawa & Tanaka, 1994) are also recessive to the normal phenotype.…”