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Drosophila Embryo Downloaded from genesdev.cshlp.org on September 24, 2021 - Published by Cold Spring Harbor Laboratory Press The decapentaplegic gene is required for dorsal-ventral patterning of the Drosophila embryo Vivian F. Irish 1 and William M. Gelbart Department of Cellular and Developmental Biology, Harvard University, Cambridge, Massachusetts 02138-2097 USA The decapentaplegic gene (dpp), which encodes a growth factor-like protein (Padgett et al. 1987), is implicated in several morphogenetic events in Drosophila melanogaster. We define here a novel embryonic function encoded by dpp m~+ alleles of the dpp gene. dpld~ null homozygotes die as ventralized embryos, dpp m~ activity is not required in the maternal germ line since lack of dpp n~ function during oogenesis has no effect on the zygotic phenotype. Since dpld~ null embryos are already abnormal early in gastrulation, the dpp m~ product is an early-acting, strictly zygotic function involved in establishing the embryonic dorsal-ventral pattern. Several maternally acting dorsalizing genes are thought to be required for the establishment of a dorsal-ventral morphogenetic gradient (Anderson et al. 1985b). We have examined the interactions of dpp m~ mutations with three of these genes. Embryos null for dpp m~ and derived from a mother homozygous for a dorsalizing mutation exhibit a lateralized phenotype, indicating that the dorsal-ventral identity of the epidermis in part derives from the direct or indirect regulation of dpp m~ activity by these genes. [Key Words: Decapentaplegic; dorsal-ventral patterning; Drosophila; embryogenesis] Received April 22, 1987; revised version accepted August 5, 1987. The establishment of the embryonic body pattern in of the decapentaplegic gene (dpp) and show that this re- Drosophila melanogaster depends on the complex inter- gion is required for dorsal epidermal tissue formation in play between maternal products and zygotic genes. A the embryo. number of maternally acting genes required for the for- Our earlier studies on dpp have defined three func- mation of the embryonic dorsal-ventral pattern have tionally distinct regions: dpp ask, dpp shy, and dpp Hin (Fig. been identified and characterized (Anderson and Nfiss- 1) (Spencer et al. 1982; Segal and Gelbart 1985; note our lein-Volhard 1984a, b). A loss-of-function mutation in revised nomenclature described in Materials and any of these loci results in a dorsalized embryonic phe- methods). Functions encoded in the imaginal disk spe- notype in which the embryo consists of an elongate tube cific (dpp d~sk) portion are required for normal adult pat- covered with dorsal cuticle. This alteration is due, at tern formation (Spencer et al. 1982). Mutations in the least in the case of dorsal, to a shift in the dorsal-ventral dpp d~sk region principally result in deletion of pattern el- pattern such that all cells acquire a more dorsal identity ements of the adult epidermal tissues derived from the (N/isslein-Volhard et al. 1980). Several biochemical and imaginal disks. In general, increasingly severe dpp d~sk genetic studies have begun to define the maternal gene mutations result in the loss of correspondingly more products required to establish the embryonic dorsal- imaginal disk-derived tissue. The relationship of the de- ventral pattern (Anderson and Nfisslein-Volhard 1984a; leted pattern elements to their imaginal disk fate map Anderson et al. 1985a). However, only a few zygotic positions has led to the suggestion that the dpp ask region genes involved in interpreting this information have may be involved in positional specification along the been identified. These include zerkniillt, tolloid, and proximo-distal axis of the developing imaginal disks shrew, which are required for the formation of dorsally (Spencer et al. 1982). Mutations in the shortvein (dpp shy) derived tissues (Jurgens et al. 1984; Wakimoto et al. region elicit head and wing venation defects, and most 1984), and twist and snail, which are necessary for the dpp ~av alleles result in larval lethality (Segal and Gelbart formation of the ventrally derived mesoderm (Simpson 1985). Lying between the dpp ~h~ and dpp d~k regions is a 1983; N6sslein-Volhard et al. 1984). Here we define a haplo-lethal region termed dpp nin (Haplo-insufficiency novel zygotic function encoded within the dpp Hm region near decapentaplegic; Spencer et al. 1982; Segal and Gel- bart 1985). Animals carrying only one wild-type copy of IPresent address: Department of Genetics, University of Cambridge, this region die during embryogenesis. Two recessive em- Cambridge CB2 3EH, UK. bryonic lethal dpp alleles have been identified on the 868 GENES & DEVELOPMENT 1:868-879 © 1987 by Cold Spring Harbor Laboratory ISSN 0890-9369/87 $1.00 Downloaded from genesdev.cshlp.org on September 24, 2021 - Published by Cold Spring Harbor Laboratory Press Dorso-ventral patterning .,_. Q. {3. "O t'~ ¢'~ lesions in maternally expressed "dorsalizing" genes, A ~'~3 ~-O 003 128 which result in the replacement of ventral with dorsal II II //-4ol pattem elements (Anderson and Nfisslein-Volhard mo oom o ~. m. 1984b). We have examined the phenotypes of animals lacking matemal activity for any of three dorsalizing genes as well as for zygotic dpp Hi" expression. The later- B alized phenotypes of embryos of these double-mutant combinations demonstrate that embryonic lateral epi- dermal tissue can be formed, even in the absence of the maternal dorsalizing gene products. These results, to- gether with observations on in situ patterns of embry- dpp onic expression of dpp transcripts (St. Johnston and Gel- ,11 Ii, bart 1987), suggest that dpp Hi" activity is required early I shy Hin I disk in development for formation of dorsal epidermal tissue. - 5' = 3' RNAs Results Generation of dpp ~n mutations / dpp H~ mutations were generated utilizing three dif- ferent protocols (see Materials and methods). Because alternative common exons 5' exons deficiencies that remove the dpp H~ region display domi- =- protein coding region nant embryonic lethality, all three schemes incorpo- rated an extra copy of dpp Hi" + so that potentially haplo- Figure 1. Chromosomal maps of the decapentaplegic (dpp) re- lethal mutations would be recoverable among some gion. (A) A linkage map of the second chromosome, indicating progeny classes. One protocol was in essence an F2 lethal the recombinational positions of several flanking markers em- screen focusing on mutations allelic to a tester recessive ployed in these experiments (see Materials and methods) dpp H~ mutation. (Lindsley and Grell 1968). (B) A genetic and molecular map of the dpp gene. dpp, located distally on the left arm of chromo- The other two protocols were F1 screens for morpho- some 2 in polytene region 22F1-2, has been subdivided into logical mutations (heldout wings), which took advantage three regions based on genetic and molecular criteria (Spencer of the following observations. Given the similarity in et al. 1982; Segal and Gelbart 1985; Gelbart et al. 1985; see lethal phenotype between homozygotes for the recessive Materials and methods for revisions to dpp nomenclature). embryonic lethal dpp alleles and monosomics for Above the map are noted the locations and extents of four rear- dpp ~+, Spencer et al. (1982) suggested that these reces- rangements used in the present studies, dpp a-h° is a 2.7-kb dele- sive alleles are leaky dpp Hm- mutations. The recessive tion (Blackman et al. 1987) that confers a recessive heldout embryonic lethal alleles partially inactivate functions of wing phenotype. Dp(2;2)dpp a21 and Dp(2;2)DTD48 are two the dpp "~sk region. If these recessive embryonic lethal dpp u~+ duplications that lack dppa°+ function, whereas dpp alleles do indeed represent hypomorphic mutations Df(2L)DTD2 removes the entire dpp gene and surrounding se- quences. Below the map, the orientation and extent of several of the haplo-lethal function, we inferred that, in the species of polyadenylated dpp transcripts are noted. These tran- presence of dpp Hm+ dpp ask- duplications, dominant scripts share exons derived from the dpp ~" region, but possess haplo-lethal mutations could be recovered on the basis different 5'-untranslated exons (St. Johnston and Gelbart 1987~ of F1 adult dpp ask phenotypes. Padgett et al. 1987; R.D. St. Johnston, pets. comm.). Using both the F1 and F2 protocols, 20 dpp lesions were identified (Table 1). Three are standard mutations in the dpp a~k region, whereas another eight are gross de- basis of allelism to dpp asa lesions; by complementation letions of dpp. Nine behave as if they are lesions within mapping, they are inseparable from the dpp n~ region the dpp Hm region. One of these nine alleles, dpp ~Sz, com- (Spencer et al. 1982). These two recessive lethal muta- pletely complements mutations of the dpp shy and dpp ~sk tions (which we will refer to as dpp b~~ mutations) are regions and therefore isgiven a special designation (dpp e allelic to most dpp °~sk and dpp shy lesions; occasional for embryonic). The other eight behave as if they par- cases of partial complementation have been shown to be tially or fully inactivate the functions of these other re- synapsis-dependent (Gelbart 1982; Wu 1984). gions of dpp. We describe the isolation of dominant haplo-lethal Embryonic phenotypes elicited by dpp ~n mutations dpp n~ mutations and the embryonic phenotypes pro- duced by these mutations as well as by recessive embry- The cuticular pattern generated during embryonic devel- onic lethal dpp lesions. Complete loss of dpp nm activity opment contains a number of recognizable structures results in a striking "ventralized" embryonic phenotype, that define both the position and the polarity of the un- in which the normally ventral epidermal pattern ele- derlying epidermis (Fig. 2A, B). Although the cuticle is ments are present both ventrally and dorsally. We not deposited until late in embryogenesis, its mor- present experiments indicating that this phenotype is phology can reflect a variety of pattern alterations due to strictly zygotic expression.
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