The interplay between multiple enhancer and silencer elements defines the pattern of decapentaplegic expression.

Abstract

The product of the zygotically active decapentaplegic (dpp) gene appears to function as a morphogen that specifies positional information in the dorsal half of the Drosophila embryo. The dorsal-specific transcription of dpp is the key step in establishing a morphogen gradient. We demonstrate here that multiple regions

Embryonic expression patterns of the drosophila decapentaplegic gene: Separate regulatory elements control blastoderm expression and lateral ectodermal expression

“…dpp mutant alleles that specifically affect either the dorsal blastoderm expression or the later lateral ectoderm expression are not yet available, so it is not known how each of these parts of the dpp expression pattern contributes to the final dorsal/ventral polarity of the embryonic cuticle. The regulatory regions defined here and by others (Huang et al, 1993) will be used to construct transgenes which in otherwise dpp null mutant backgrounds will allow the contribution of the dorsal blastoderm expression and the later lateral stripe expression to be assessed independently.…”

“…Expression from the P[dpp83-87, lac] transgene indicated the presence of essential regulatory elements within the dpp second intron. Using different constructs, Huang et al (1993) also found regulatory elements in the second intron of dpp.…”

Efficient studies of long-distance Bmp5 gene regulation using bacterial artificial chromosomes

“…For example, detailed molecular and genetic studies have shown that different aspects of Drosophila melanogaster decapentaplegic (dpp) gene expression are regulated by distinct sequences. Expression of the gene in the midgut is controlled by sequences located 5Ј of the gene (1,2), early embryonic expression by sequences in the intron (3), and imaginal disk expression by sequences located 3Ј of the coding sequences (4)(5)(6). Even in the relatively compact fly genome, some of the dpp enhancers are located more than 30 kb from the promoter.…”

Model Organisms in the Study of Development and Disease

“…The absence of Dorsal defines the nonneural ectoderm by virtue of Dorsal acting as a repressor of dorsally expressed genes such as dpp and zen in ventral and lateral cells (Rushlow et al, 1987;Doyle et al, 1989;Ray et al, 1991;Jiang et al, 1992Jiang et al, , 1993Huang et al, 1993Huang et al, , 1995. The key gene involved in development of dorsal cells is dpp, the homolog of vertebrate BMP2/4 (Padgett et al, 1987).…”

“…High levels of Dorsal are required for activating expression of mesoderm-determining genes such as snail Leptin, 1991;Rao et al, 1991;Ray et al, 1991;Thisse et al, 1991;Ip et al, 1992b) and twist (Jiang et al, 1991;Kosman et al, 1991;Leptin, 1991;Rao et al, 1991;Ray et al, 1991), whereas lower levels are required to activate genes such as rhomboid (rho) Leptin, 1991;Rao et al, 1991;Ray et al, 1991;Ip et al, 1992a), ventral nervous system defective (vnd) (Mellerick and Nirenberg, 1995), intermediate nervous system defective (ind) (McDonald et al, 1998;Weiss et al, 1998), short gastrulation (sog) (Francois et al, 1994), and brinker (brk) (Jazwinska et al, 1999a(Jazwinska et al, , 1999b in the neuroectoderm. The absence of Dorsal defines the dorsal domain since Dorsal represses expression of key genes required for the establishment of dorsal cell fates, such as decapentaplegic (dpp) (Ray et al, 1991;Jiang et al, 1993;Huang et al, 1993Huang et al, , 1995, zerknüllt (zen) (Rushlow et al, 1987;Doyle et al, 1989;Ray et al, 1991;Jiang et al, 1992), tolloid (tld) (Kirov et al, 1994), and twisted gastrulation (tsg) (Mason et al, 1994).…”