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Allele Dmel\ecd¹

General Information
Symbol	Dmel\ecd1	Species	D. melanogaster
Name		FlyBase ID	FBal0003500
Feature type	allele	Created / Updated	2006-08-22/2006-08-22
Associated gene	Dmel\ecd
Allele class	amorph, hypomorph
Mutagen	ethyl methanesulfonate
Nature of the Allele
Allele class	amorph (Furia et al., 1992) hypomorph (Henrich et al., 1993)
Mutagen	ethyl methanesulfonate (Belinski-Deutsch et al., 1983)
Mapped Features and Mutations
Type Symbol & Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion	Statement Reference Amino acid replacement: P656S. (Gaziova et al., 2004)
Assay mode
Cytology
Phenotypic Data
Phenotypic Class
	lethal | recessive | conditional - heat sensitive (James and Collier, 1990, Belinski-Deutsch et al., 1983) lethal | conditional - heat sensitive (Farkas and Knopp, 1997) lethal | embryonic stage | conditional - heat sensitive (Kozlova and Thummel, 2003) lethal | larval stage (Gaziova et al., 2004) lethal | larval stage (with Df(3L)R-R2) (Gaziova et al., 2004) lethal | larval stage (with ecd2) (Gaziova et al., 2004) lethal | larval stage (with ecdl(3)23) (Gaziova et al., 2004) lethal | larval stage | recessive | conditional - heat sensitive (Dai et al., 1991, Henrich et al., 1993, Martinez-Padron and Ferrus, 1997) lethal | pharate adult stage | conditional - heat sensitive (Sliter, 1987) visible | recessive | conditional - heat sensitive (Brennan et al., 1998) female sterile | recessive | temperature conditional (Bai et al., 2000) female sterile | recessive | conditional - heat sensitive (Belinski-Deutsch et al., 1983) short lived (Berreur et al., 1984) neuroanatomy defective | larval stage | recessive | conditional - heat sensitive (Martinez-Padron and Ferrus, 1997) immune response defective | recessive | conditional - heat sensitive (Sorrentino et al., 2002) immune response defective | conditional - heat sensitive (with Df(3L)R-G7) (Sorrentino et al., 2002)
Phenotype Manifest In
	lymph gland (with Df(3L)R-G7) (Sorrentino et al., 2002) eye | conditional - heat sensitive (Brennan et al., 1998) morphogenetic furrow | conditional - heat sensitive (Brennan et al., 1998) egg chamber (Petavy, 1991, Petavy, 1990, Bai et al., 2000) nurse cell (Petavy, 1991) follicle cell (Petavy, 1991, Petavy, 1990) yolk (Petavy, 1991) egg (Petavy, 1991, Petavy, 1990) blastoderm embryo (Petavy, 1991) stomodeal invagination (Petavy, 1991) amnioproctodeal invagination (Petavy, 1991) extended germ band embryo (Petavy, 1991, Kozlova and Thummel, 2003) prothoracic gland | conditional - heat sensitive (Dai et al., 1991) lamellocyte (Sorrentino et al., 2002) hemocyte (Sorrentino et al., 2002) eye-antennal disc | conditional - heat sensitive (Henrich et al., 1993) dorsal mesothoracic disc | conditional - heat sensitive (Henrich et al., 1993) ventral thoracic disc | conditional - heat sensitive (Henrich et al., 1993) macrochaeta & adult thorax | conditional ts (Henrich et al., 1993) larva (Berreur et al., 1984) vitelline membrane (Petavy, 1990) chorion (Petavy, 1990) Golgi stack | conditional - heat sensitive (Kondylis et al., 2001) dorsal closure embryo (Kozlova and Thummel, 2003) embryonic/first instar larval cuticle (Kozlova and Thummel, 2003) border follicle cell (Bai et al., 2000) synapse | conditional - heat sensitive (Martinez-Padron and Ferrus, 1997) mouth hooks (with ecd2) (Gaziova et al., 2004) mouth hooks (with Df(3L)R-R2) (Gaziova et al., 2004) mouth hooks (with ecdl(3)23) (Gaziova et al., 2004)
Detailed Description
	Statement Reference temperature-sensitive recessive lethal. At 29oC, the nine-fold increase in β-ecdysone content during embryogenesis occurs normally in ecd homozygotes. Accompanied by normal increases in dopa-decarboxylase and dopamine acetyltransferase activity (Marsh and Wright, 1980). The four-fold increase during the first larval instar is reduced to 40% of normal; the additional twelve-fold increase normally occurring at pupariation eliminated. embryonic lethal. Embryonic development of ecd at 29oC normal, but first larval molt delayed and death usually occurs by end of second instar; shift down to 20oC at mid second instar produces full yield of adult progeny. Larvae shifted from 20oC to 29oC midway through third instar fail to pupate and survive as larvae for up to 3 weeks; ring gland, salivary glands and brain of nonpupariating larvae are smaller than wild type; such ring glands cultured in vitro secrete ecdysone at lower than normal levels. Effects of 29oC on third instar reversible by ecdysone feeding or by shift down to 20oC within 3-5 days of shift up; after that imaginal discs cannot differentiate; ecd imaginal discs develop normally at 29oC when implanted in a wild-type host. A heat pulse during larval development results in cell death with consequent abnormalities in emerging adults. At 29oC, third instar larvae exhibit abnormally low dopadecarboxylase activity (Kraminsky, Clark, Estelle, Gietz, Sage, O'Connor and Hodgetts, 1980); Marsh and Wright, 1980) and high urate oxidase activity (Krase and Friedman, 1979); ecdysone feeding effects normal levels. Transfer to restrictive conditions at the beginning of the pupal stage leads to death as pharate adults and to the elimination of mechanosensory chaetae; Non-sensory chaetae and other sensilla not affected. Chaetae loss is autonomous as seen in homozygous clones produced by somatic exchange and in ecd discs passed through metamorphosis in wild type hosts under restrictive conditions (Sliter, 1989). Sensitivity to restrictive temperature disappears in 24 hour pupae. ecd fails to block midpupal increase in ecdysone titer (Marsh and Wright, 1980). Shifting newly emerged ecd adults to 29oC results in drastically reduced ecdysone titers and sterilizes both males and females; reversible by shift back to 20oC; temperature-sensitive periods and therefore the times that ecdysone is required for embryonic development, chorion formation, and vitellogenesis are 1-2 days before oviposition, 24 hr prior to oviposition, and prior to stage 7, respectively (Audit-Lamour and Bussin, 1981).   Homozygotes shifted to 29oC at puparium formation die at emergence, although the mid-pupal peak of ecdysteroids is unaffected in these animals. Homozygotes shifted to 29oC 24 hours before pupariation exhibit a significant decrease in the mid-pupal peak of ecdysteroids, although the pupariation peak is unaffected. These animals die before emergence, but after the mid-pupal ecdysteroid peak. (Belinski-Deutsch et al., 1983) Most homozygous larvae transferred to the restrictive temperature of 29oC at the end of the second larval instar die before pupariation without reaching full growth. Larvae transferred to 29oC during the 30 hours after the second molt show variable behaviour; some form a normally tanned puparium but pupal development is arrested, some die as fully elongated larvae with partial darkening of the cuticle, and some remain as active larvae. Larvae transferred to 29oC immediately at the second molt remain as active, permanent larvae. These larvae do not leave the food, reach a maximum weight greater than wild-type larvae and contain low levels of ecdysteroids compared to wild-type. Returning the larvae to a permissive temperature (20oC) does not induce normal pupariation. Feeding with a 20-hydroxyecdysone-yeast mixture triggers abortive pupariation. Larvae maintained at 27.5oC have nearly normal levels of ecdysteroids. (Berreur et al., 1984) Defective imaginal disc development. (Sliter, 1987) Ovarian development becomes severely disturbed and oogenesis gradually declines in a few days in newly eclosed homozygous females transferred to 29oC. Follicles begin to degenerate, mainly at stage 9 and enlarged agametic chambers become conspicuous (in the absence of the oocyte, the nurse cells keep on growing until they degenerate, while some follicle cells die). In other egg chambers the yolk deposition starts then slows down and stops, and local cell death followed by general degeneration of the follicle occurs. Five days after the temperature shift to 29oC some females lay a few eggs which are flaccid and/or translucent. When oviposition has stopped, the degenerating ovarian chambers are piled up within the tubular sheath of each ovariole. Mature homozygous flies transferred to 29oC also show disruptions in ovarian functioning; the frequency of aberrant previtellogenic follicles steadily increases, cell death occurs in increasing numbers of follicles, both germinal and somatic cells die and disintegrate, follicles become disorganised, and eggs have defective eggshell layers, appearing flaccid and translucent. (Petavy, 1990) At 29oC the prepupal activity peak of Argk is not seen. At 20oC the activity peak reappears. At the restrictive temperature imaginal discs progressively lose Argk gene product activity. (James and Collier, 1990) The prothoracic gland cells of homozygous larvae shifted to 29oC show a number of ultrastructural abnormalities, including a decrease in the invaginations of the plasma membrane, an accumulation of lipid droplets in the cytoplasm, lack of smooth endoplasmic reticulum, an increase in the amount of rough endoplasmic reticulum and highly electron-dense mitochondria. The prothoracic glands produce only about 16% of the level of ecdysteroids synthesised by wild-type glands at 29oC. The corpus allatum appears normal at 29oC. The prothoracic gland defects are also seen in prothoracic glands dissected from larvae reared at 18oC and then cultured in vitro for 4 hours at 29oC. (Dai et al., 1991) Homozygous females develop multiform ovarian dysfunctions within a few days of being transferred to 29oC. The first defects are detected well before vitellogenesis, and include egg chambers which lack the oocyte, although the nurse cells grow normally, abnormal numbers of nurse cells and a flattened follicular epithelium. Follicle polarity may be abnormal, with the oocyte being lateral instead of posterior. Mid-stage follicles are also abnormal, with pyknosis in the nuclei of follicular and nurse cells, followed by gradual disorganisation of the somatic and germline derivatives. Live cells may be close to degenerated ones in the same egg chamber. About half of stage 13-14 follicles or newly laid eggs appear highly disorganised, with irregular thickness of the yolk-free peripheral cytoplasm and/or abnormal distribution of the yolk bodies. The newly laid eggs often appear flaccid and translucent, with the proportion increasing as the time after the temperature shift of the females to 29oC increases. The eggs are reduced in volume and length compared to wild-type. Stage 12 to 14 oocyte envelopes are permeable to Fe3+ ions. Multiform defects are seen over the first half of embryogenesis; pseudocleavage may occur during the first 2 hours - cytoplasmic islands devoid of nulcei or chromosomes emerge within the yolk mass. Invasion of the peripheral cytoplasm by cleavage nuclei is incomplete and/or there may be local degeneration of some blastoderm nuclei. Abnormal morphogenetic movements are seen during gastrulation, formation of the midgut invaginations, germband elongation and segmentation. (Petavy, 1991) Temperature-sensitive allele. Histolysis of the larval fat body at the restrictive temperature of 29oC is the same in heterozygotes and homozygotes. (Richard et al., 1993) Homozygotes reared continuously at the restrictive temperature survive to the third larval instar stage. These larvae appear to lack both eye-antennal and mesothoracic discs, and leg discs are reduced in size. Hemizygous larvae survive through to the late second instar stage, but die suddenly before moulting. ecd1/ecd2 transheterozygotes die as they moult to the third larval instar; most die during ecdysis, with the old cuticle often remaining attached to the posterior end of the abdomen. Only 0.7% of eggs from a cross between ecd3D/+ females and ecd1/+ males hatch as ecd1/ecd3D larvae at 29oC. These infrequent survivors die shortly after hatching. 7.3% of eggs from a cross between ecd3D/+ males and ecd1/+ females hatch as ecd1/ecd3D larvae at 29oC. The number of macrochaetae on the thorax is reduced in homozygous and hemizygous ecd1 flies, and in ecd1/ecd2, ecd1/ecdg4, ecd1/ecdg6, ecd1/ecdg5 and ecd1/ecd3D flies kept at 29oC in the hours that follow prepupal formation. (Henrich et al., 1993) The mutant shows changes in the amounts, and differences in ratios of particular, of cuticular hydrocarbons compared to the wild-type (at both permissive and restictive temperatures). (Wicker and Jallon, 1995) Homozygotes fail to produce the precursor of 20-hydroxyecdysone at the non-permissive temperature (29oC). (Spiegelman et al., 1997) Larvae fail to pupate when transferred to 30oC midway through third instar. They remain as larvae for an extended period of time and develop enlarged type III synaptic boutons. (Martinez-Padron and Ferrus, 1997) Mutant larvae develop relatively normally at the restrictive temperature of 29oC, but are unable to pupariate. (Awad and Truman, 1997) Homozygotes show eye defects when shifted to 30oC for 24 hours during the third larval instar stage. ecd1/Df(3L)R-G7 larvae exposed to 30oC for 24 hours during the third larval instar stage and then shifted to the permissive temperature (18oC) develop into adults with defects in the eye and anterior nicks in the retinal tissue. Progression of the morphogenetic furrow is disrupted; the furrow is either slowed or stopped and is also dysmorphic. Cell proliferation ahead of the furrow is not visibly altered, but cell-cycle synchrony in the furrow is lost. No excess cell death is seen. Animals exposed to 30oC for 24 hours during the second larval instar stage have more severe eye defects, with intrusions of cuticle into the eye field. (Brennan et al., 1998) The temperature-sensitive lethality of ecd1 animals can be partially rescued by exogenous application of the compounds 20-hydroxyecdysone, RH-5849 and RH-5992; the compounds can stimulate abortive pupariation in the animals maintained at the restrictive temperature from the third larval instar stage. (Farkas and Slama, 1999) Homozygous females are sterile if held at the nonpermissive temperature for 5 days, and egg chambers in these flies arrest development at stage 8 and subsequently degenerate. Border follicle cells fail to develop in these arrested egg chambers. When mutant females are held at the nonpermissive temperature for 2 days, some stage 10 egg chambers develop, in which border cells differentiate. More than 50% of these egg chambers show delayed border cell migration. (Bai et al., 2000) Mutant larvae transferred to 29oC (the restrictive temperature) for 7 hours at 6 days after egg laying at 22oC and then maintained at 29oC for 18 hours show larval clusters of vesicles and tubules in the Golgi areas of leg and wing discs. Mutant larvae maintained at 29oC for 7 hours and then transferred to 22oC for 18 hours show neatly stacked cisternae in the Golgi areas of the discs. Discs dissected from larvae maintained at 29oC for 6 hours and incubated at 22oC in the absence of ecdysone show larval clusters in the Golgi areas, whereas those incubated in the presence of ecdysone show stacked cisternae. (Kondylis et al., 2001) ecd1/Df(3L)R-G7 larvae show lymph gland hypertrophy and failure to pupariate when raised at 27oC. ecd1 homozygotes and ecd1/Df(3L)R-G7 mutants exhibit a total and near total loss of encapsulation capacity when challenged with L. boulardi G486. Lamellocytes appearing in response to parasitization are reduced to zero or near zero. ecd1/Df(3L)R-G7 mutants also show a significant reduction in the frequency of lymph gland dispersal in parasitized individuals. Parasitised mutant lymph glands fail to show the hemocyte mitotic burst characteristic of wild type. Lymph glands of older, developmentally arrested mutant larvae are larger and show a temperature dependent hypertrophy. The greatest degree of hypertrophy is seen in the posterior lobe. Parasitisation does not disperse the lymph glands. Parasitised mutant lymph glands show a near normal increase in population size of crystal cells. (Sorrentino et al., 2002) ecd1 animals maintained at the non-permissive temperature show defects in germ band retraction, head involution and cuticle deposition. (Kozlova and Thummel, 2003) ecd1 homozygotes die between L2 and mid L3. Most ecd1/Df(3L)R-R2, ecd1/ecd2 or ecd1/ecdl(3)23 animals die during the L2/L3 molt, displaying typical molting defects such as double mouth hooks, but some survive into L3. Larval lethality of ecd1 homozygous larvae is rescued by feeding with 20-hydroxyecdysone at 29oC. (Gaziova et al., 2004)
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Statement Reference ecd1 is a suppressor | partially of immune response defective | conditional - heat sensitive phenotype of hopTum (Sorrentino et al., 2002) ecd1 is a suppressor | partially of melanotic 'tumor' | conditional - heat sensitive phenotype of hopTum (Sorrentino et al., 2002)
Phenotype Manifest In
Enhanced by
Statement Reference B1, ecd1 has eye phenotype, enhanceable by trr1 (Sedkov et al., 2003)
Other
Statement Reference ecd1, l(2)glts3 has larva phenotype (Manfruelli et al., 1996) ecd1, l(2)glts3 has dorsal mesothoracic disc phenotype (Manfruelli et al., 1996) B1, ecd1 has eye phenotype (Sedkov et al., 2003)
Additional Comments
Genetic Interactions
Statement Reference Lowering of ecdysone levels in hopTum/Y; ecd1/ecd1 resulted in mild suppression of the hopTum melanotic capsule phenotype and the encapsulation capacity on parasitisation by L. boulardi G486. (Sorrentino et al., 2002) In animals that are homozygous for ecd1 and are also B1 the addition of trr1 enhances the eye phenotype. (Sedkov et al., 2003)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Fails to complement	ecdg6 (Henrich et al., 1993) ecdg5 (Henrich et al., 1993) ecdg4 (Henrich et al., 1993) ecd3D (Henrich et al., 1993)
Rescued by	ecd1/ecdg24 is rescued by ecd+tE5 (Gaziova et al., 2004) ecd2/ecd1 is rescued by ecd+tE5 (Gaziova et al., 2004) ecd1/ecdg24 is rescued by ecd+tS4 (Gaziova et al., 2004) ecd2/ecd1 is rescued by ecd+tS4 (Gaziova et al., 2004)
Comments	Fails to complement ecd3D, ecdg4, ecdg5 and ecdg6 at 29oC, although ecd1/ecd3D, ecd1/ecdg4, ecd1/ecdg5 and ecd1/ecdg6 animals complete development at 18oC. (Henrich et al., 1993)
Stocks ( 4 )
Bloomington	218 ecd1 st1 ca1 4210 ecd1 st1 red1 e4 ca1
Kyoto	105795 ecd1 st1 ca1 107633 ecd1 st1 red1 e4 ca1
Notes on Origin
Discoverer
Comments
	The temperature sensitive period (TSP) for the decrease in the ecdysteroid mid-pupal peak occurs before pupariation. There are two TSPs for lack of emergence; one before and one just after pupariation. (Belinski-Deutsch et al., 1983) All aspects of mutant phenotype can be rescued in 35% homozygotes by Tp(3;Y)H141. (Sliter, 1987) In wild type Adh mRNA levels decrease and Gld mRNA levels and enzyme activity increase upon treatment with an exogenous source of ecdysterone. This is reversed in ecd-1 larvae, no decrease in Adh mRNA level or increase in Gld mRNA level is seen. (Murtha and Cavener, 1989) Mid third instar larvae at 29oC do not exhibit the pre-pupal peak of Argk activity. The peak reappears if larvae are shifted to 20oC or are fed 20-HE. (James and Collier, 1990)
Synonyms & Secondary IDs ( 11 )
Reported As
Symbol Synonym	ecd-1 (Roth et al., 2004, Belinski-Deutsch et al., 1983, Takeuchi et al., 2005) ecd1 (Kozlova and Thummel, 2003) ecd1ts (Antoniewski et al., 1994) ecd-1ts (Petavy, 1991, Petavy, 1990, Deutsch et al., 1989) ecd1 (Willard et al., 2006, Lovato et al., 2005, Christensen et al., 2007.10.29, Christensen et al., 2007.10.29) ecd1ts (Kondylis et al., 2001, Laval et al., 1993, Dai et al., 1991) ecdlts (Maschat et al., 1991) l(3)ecd1 (Bonnette et al., 1996) l(3)ecd-1ts (Berreur et al., 1984) l(3)ecd1 (Kozlova and Thummel, 2000, Buszczak et al., 1999, Buszczak et al., 1998, Warren et al., 1996)
Name Synonym	ecdysoneless 1ts (Ferveur, 1997)
Secondary FlyBase IDs
References ( 61 )
Generate a list of	All references relating to this allele ( 61 )
List References by type	Research paper  ( 48 ) Supplementary material  ( 1 ) Review  ( 4 ) Personal communication to FlyBase  ( 2 ) Abstract  ( 5 ) Letter  ( 1 )
Recent research papers ( 1 )
	Willard et al., 2006, Dev. Biol. 296(1): 150--163 Chronic cocaine exposure in Drosophila: life, cell death and oogenesis. [FBrf0193254] Show all research papers ...
Recent reviews (0)
	All reviews listed in FlyBase were published before 2006 Show reviews ...