scholarly journals THE INTERACTION OF TWO COMPLEX LOCI, ZESTE AND BITHORAX IN DROSOPHILA MELANOGASTER

Genetics ◽  
1973 ◽  
Vol 75 (2) ◽  
pp. 299-321
Author(s):  
T C Kaufman ◽  
S E Tasaka ◽  
D T Suzuki

ABSTRACT It has been found that certain alleles of the zeste locus (za 1-1.0) have no phenotype of their own, but interact with certain alleles at the bithorax locus (bx 3-58.8). This interaction takes the form of an enhancement of the homeotic bx phenotype to a more extreme form—i.e., the metathorax is transformed into mesothorax in varying degrees depending on the bx allele used. This enhancement is somewhat reminiscent of the transvection effect described by Lewis (1954). The characterization of the interaction thus far has shown that the enhancement only effects bx alleles which arise spontaneously, whereas the origin of the za allele is unimportant. The gene claret nondisjunctional was used for the production of gynandromorphs which showed that the enhancing ability of za, like the eye pigment change caused by z, is autonomous. The enhancement of one specific allele (bx34e), which is temperature-sensitive, has allowed a delineation of the temperature-sensitive period of the bithorax locus to a period extending from the middle of the second larval instar to the middle of the third larval instar. These results, as well as those of other enhancer and suppressor systems in Drosophila, have revealed the possibility of the involvement of heterocyclic compounds in the control of cell determination and fate in Drosophila melanogaster.

1984 ◽  
Vol 54 (1) ◽  
pp. 76-84 ◽  
Author(s):  
P. Berreur ◽  
P. Porcheron ◽  
M. Moriniere ◽  
J. Berreur-Bonnenfant ◽  
S. Belinski-Deutsch ◽  
...  

1978 ◽  
Vol 31 (1) ◽  
pp. 73
Author(s):  
CR Datson ◽  
NG Brink

A new X-linked temperature-sensitive female sterile mutant (/(1)1074") is described. The nonpermissive temperature for this mutant is 29�C. There are two temperature-sensitive periods during development-one between the 6th and 12th hours of embryogenesis and a second commencing during the first larval instar and terminating at mid pupation. Embryological abnormalities first become apparent during gastrulation and eventually these result in the breakdown of organogenesis and the complete absence of normal muscular contractions. Preconditioning mutant females at the nonpermissive temperature for up to 48 h enhances the abnormal embryological effects produced by the mutant.


1957 ◽  
Vol s3-98 (41) ◽  
pp. 123-150
Author(s):  
JOAN M. WHITTEN

The fate of the tracheal system is traced from the first larval instar to the adult stage. The basic larval pattern conforms to that shown for other Diptera Cyclorrhapha (Whitten, 1955), and is identical in all three instars. According to previous accounts the adult system directly replaces the larval: the larval system is partly shed, partly histolysed, and the adult system arises from imaginal cell clusters independently of the preceding larval system. In contrast, it is shown here that in the cephalic, thoracic, and anterior abdominal region there is a definite continuity in the tracheal system, from larval, through pupal to the adult stage, whereas in the posterior abdominal region the larval system is histolysed, and the adult system is independent of it in origin. Moreover, in the pupal stage this region is tracheated by tracheae arising from the anterior abdominal region and belonging to a distinct pupal system. Moulting of the tracheal linings is complete at the first and second larval ecdyses, but incomplete at the third larval-pupal and pupal-adult ecdyses. In consequence, in both pupal and adult systems there are tracheae which are secreted around preexisting tracheae, others formed as new ‘branch’ tracheae, and those which have been carried over from the previous instar. In the adult the newly formed tracheae of the posterior abdominal region fall into a fourth category. Most of the adult thoracic air sacs correspond to new ‘branch’ tracheae of other instars. The pre-pupal moult and instar are discussed with reference to the tracheal system and tentative suggestions are made concerning the true nature of the pre-pupal cuticle. There is no pre-pupal tracheal system. Events traced for Drosophila would seem to be general for Cyclorrhapha, both Acalypterae and Calypterae. The separate fates of the anterior and posterior abdom inal systems, in contrast with the straightforward development in Dipterc Nematocera, would appear to mark a distinct step in the evolution of the system in Diptera.


Heredity ◽  
2009 ◽  
Vol 104 (2) ◽  
pp. 125-134 ◽  
Author(s):  
K S Pedersen ◽  
M C Codrea ◽  
C J Vermeulen ◽  
V Loeschcke ◽  
E Bendixen

1972 ◽  
Vol 20 (1) ◽  
pp. 115-135 ◽  
Author(s):  
Ann Louise Belt ◽  
Barrie Burnet

SUMMARYThe melanotic tumour gene tu-C4 in Drosophila melanogaster shows incomplete dominance, together with variable penetrance and expressivity. It is tentatively located in the region of locus 52–53 on the third chromosome. Tumour formation in mutant homozygotes involves a precocious haemocyte transformation leading to the appearance of lamellocytes at the beginning of the third larval instar. These aggregate to form tumour-like masses which subsequently melanize. The process of tumour formation is in broad outline similar to that found in other tumour strains. Melanotic tumour formation is treated as a dichotomous threshold character, assuming an underlying normal distribution of liability relative to a fixed threshold. The expression of the tumour gene can be influenced by the levels of protein, phospholipid, nucleic acid and carbohydrate in the larval food medium, and changes in dominance and penetrance induced by sub-optimal environments deficient in these nutrients are positively correlated. Reinforcement by selection of the dominance relations of tu-C4 was accompanied by correlated changes in penetrance. Conversely, selection for increased penetrance was accompanied by correlated changes in dominance. Dominance and penetrance, it is concluded, are fundamentally related aspects of tumour gene expression. Recruitment of dominance modifiers linked to the tumour gene was excluded by the mating scheme employed, and the observed changes in dominance relations in response to selection were due largely to modifiers located on the second chromosome. Changes in dominance relations produced by selection could be significantly reinforced, or reversed, by environmental factors and consequently show a substantial genotype – environment interaction effect. These facts are relevant to current theories of dominance evolution.


1984 ◽  
Vol 44 (1) ◽  
pp. 11-28 ◽  
Author(s):  
Margaret G. Kidwell

SummaryVariable frequencies of unhatched eggs were observed to be produced by a number of F1 interstrain hybrids. This type of partial sterility resulting from F2 embryo death was found to be associated with the P-M system of hybrid dysgenesis. Dysgenic hybrid progeny of crosses between M strain females and P strain males may therefore have reduced fertility due to the disruption of development at two different stages: early F1 gonadal development and early F2 embryo development. These disruptions result in the previously described F1 gonadal dysgenesis (GD sterility) and F2 embryo lethality (EL sterility) respectively. The two morphologically distinct types of P-M-associated sterility differ in their patterns of response to F1 developmental temperature, and the temperature-sensitive period for EL sterility occurs considerably later in F1 development than for GD sterility. EL sterility is similar to SF sterility, which is associated with the I–R system of hybrid dysgenesis in that both result from death during early F2 embryogenesis. However, EL sterility differs from SF sterility in not being restricted to hybrids of the female sex and in showing different patterns of response to temperature and ageing in the F1 generation. Some implications of the existence of EL sterility for methods of strain classification in the I–R system are explored.


Genetics ◽  
1981 ◽  
Vol 97 (3-4) ◽  
pp. 581-606 ◽  
Author(s):  
Donald A R Sinclair ◽  
David T Suzuki ◽  
Thomas A Grigliatti

ABSTRACT A temperature-sensitive (ts) third chromosome Minute (M) mutation, designated Q-III, has been recovered and characterized. Q-III heterozygotes raised at 29" exhibit all of the dominant traits of M mutants including small bristles, rough eyes, prolonged development, reduced viability 2nd interactions with several unrelated mutations. Q-III homozygotes raised at 29° are lethal; death occurs primarily during the first larval instar. When raised at 22°, Q-Ill heterozygotes are phenotypically normal and Q-III homozygotes display moderate Mtraits. In addition, Q-IIIelicits ts sterility and maternal-effect lethality. As it true of Mlesions, the dominant traits of Q-111 are not expressed in triploid females raised at 29°. Complementation tests suggest that Q-III is a ts allele of M(3)LS4, which is located in 3L near the centromere.——Reciprocal temperature-shift experiments revealed that the temperature-sensitive period (TSP) of Q-111 lethality is polyphasic, extending from the first instar to the latter half of pupation. Heat-pulse experiments further resolved this into two post-embryonic TSPs: one occurring during the latter half of the second larval instar, and the other extending from the larval/pupal boundary to the second half of pupation. In addition, heat pulses elicited a large number of striking adult phenotypes in Q-III individuals. These included pattern alterations such as deficiencies and duplications and cther morphological defects in structures produced by the eye-antennal, leg, wing and genital imaginal discs and the abdominal histoblasts. Each defect or pattern alteration is associated with a specific TSP during development.——We favor the interpretation that most of the major Q-III defects, particularly the structural duplications and deficiencies, result from temperature-induced cell death in mitotically active imaginal anlagen, while the small macrochaete phene probably results from the direct effects of Q-III on bristle synthesis. The hypothesis that the Q-III locus specifices a component required for protein synthesis is discussed, and it is concluded that this hypothesis can account for the pleiotropy of Q-III, and that perhaps it can be extended to M loci in general.


Genetics ◽  
1988 ◽  
Vol 118 (2) ◽  
pp. 247-259
Author(s):  
I Kiss ◽  
A H Beaton ◽  
J Tardiff ◽  
D Fristrom ◽  
J W Fristrom

Abstract The 2B5 region on the X chromosome of Drosophila melanogaster forms an early ecdysone puff at the end of the third larval instar. The region contains a complex genetic locus, the Broad-Complex (BR-C) composed of four groups of fully complementing (br, rbp, l(1)2Bc, and l(1)2Bd) alleles, and classes of noncomplementing (npr 1) and partially noncomplementing l(1)2Bab alleles. BR-C mutants prevent metamorphosis, including the morphogenesis of imaginal discs. Results are presented that indicate that the BR-C contains two major functional domains. One, the br domain is primarily, if not exclusively, involved in the elongation and eversion of appendages by imaginal discs. The second, the l(1)2Bc domain, is primarily involved in the fusion of discs to form a continuous adult epidermis. Nonetheless, the two domains may encode products with related functions because in some situations mutants in both domains appear to affect similar developmental processes.


Genetics ◽  
1983 ◽  
Vol 105 (1) ◽  
pp. 55-69
Author(s):  
Joseph J King ◽  
John F McDonald

ABSTRACT A region-specific, trans-acting regulatory gene that alters in vivo protein levels of α-glycerophosphate dehydrogenase (α-GPDH) has been mapped to position 55.4 on the third chromosome of Drosophila melanogaster. The gene has been found to affect the in vivo stability of α-GPDH in adult thoracic tissue but has no effect on α-GPDH levels in the abdomen. Although no other thoracic proteins were found to be influenced by the locus, it appears to modify the level of one additional abdominal protein. The action of the gene over development and its possible mode of control are discussed.


Genetics ◽  
1974 ◽  
Vol 76 (3) ◽  
pp. 487-510
Author(s):  
Marianne E Dudick ◽  
Theodore R F Wright ◽  
Lynda Lee Brothers

ABSTRACT A temperature-sensitive lethal allele of suppressor of forked, l(1)su(f)ts67g (ts67), has been discovered and characterized as follows: Flies which are hemizygous for ts67 live at 18° and 25° but die at 30° primarily as larvae. The temperature-sensitive period for ts67 homozygotes or hemizygotes begins in second instar and ends at pupation. ts67 is lethal at 30° when heterozygous with suppressor of forked (su(f)), a deficiency for suppressor of forked (su(f)  -), and a non-conditional lethal allele of suppressor of forked (3DES). It is viable at 30° when heterozygous with the wild-type allele of suppressor of forked. At 25° but not at 18° forked bristles are suppressed in flies of the following genotypes: fsts67/Y, fsts67/fsts67, fsts67/fssu(f), futs67/fs3DES, futs67/fssu(f)  -, futs67/fssu(f). There is some suppression of forked bristles at 25° in the heterozygote, fsts67/fs+su(f). The forked bristle phenotype is not suppressed at either temperature in flies of the genotypes futs67/Y, futs67/futs67/ (fs and fu indicating suppressible and unsuppressible alleles of forked). The temperature-sensitive period for suppression of forked bristles begins at pupation and extends through the period of bristle synthesis. The deficiency phenotype (bristles reduced in size or absent, wing wrinkled or blistered, eyes rough) typical of flies of the genotype fssu(f)/fssu(f)  - at 18° and 25°, is exhibited by flies of the genotypes fsts67/fssu(f)  - at 25° and futs67/fssu(f) at 29°. An allele of lozenge (lz1) which can be suppressed by su(f) is suppressed at 25° but not at 18° in lz1ts67/Y males. ts67 homozygous females are fertile at 25° but sterile at 30°. The hypothesis is discussed that the su(f) locus codes for a ribosomal protein and that suppression and enhancement are affected by mutations at the locus by mutant ribosome-induced misreading. The possibility is presented that ts67 may be used to determine the translation time in development of any gene.


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