The Short antennae gene of Tribolium is required for limb development and encodes the orthologue of the Drosophila Distal-less protein

Development ◽  
2001 ◽  
Vol 128 (2) ◽  
pp. 287-297 ◽  
Author(s):  
A. Beermann ◽  
D.G. Jay ◽  
R.W. Beeman ◽  
M. Hulskamp ◽  
D. Tautz ◽  
...  

Insects bear a stereotyped set of limbs, or ventral body appendages. In the highly derived dipteran Drosophila melanogaster, the homeodomain transcription factor encoded by the Distal-less (Dll) gene plays a major role in establishing distal limb structures. We have isolated the Dll orthologue (TcDll) from the beetle Tribolium castaneum, which, unlike Drosophila, develops well-formed limbs during embryogenesis. TcDll is initially expressed at the sites of limb primordia formation in the young embryo and subsequently in the distal region of developing legs, antennae and mouthparts except the mandibles. Mutations in the Short antennae (Sa) gene of Tribolium delete distal limb structures, closely resembling the Dll phenotype in Drosophila. TcDll expression is severely reduced or absent in strong Sa alleles. Genetic mapping and molecular analysis of Sa alleles also support the conclusion that TcDll corresponds to the Sa gene. Our data indicate functional conservation of the Dll gene in evolutionarily distant insect species. Implications for evolutionary changes in limb development are discussed.

Open Biology ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 190245
Author(s):  
Eléanor Simon ◽  
Sergio Fernández de la Puebla ◽  
Isabel Guerrero

Specific neuropeptides regulate in arthropods the shedding of the old cuticle (ecdysis) followed by maturation of the new cuticle. In Drosophila melanogaster , the last ecdysis occurs at eclosion from the pupal case, with a post-eclosion behavioural sequence that leads to wing extension, cuticle stretching and tanning. These events are highly stereotyped and are controlled by a subset of crustacean cardioactive peptide (CCAP) neurons through the expression of the neuropeptide Bursicon (Burs). We have studied the role of the transcription factor Odd-paired (Opa) during the post-eclosion period. We report that opa is expressed in the CCAP neurons of the central nervous system during various steps of the ecdysis process and in peripheral CCAP neurons innerving the larval muscles involved in adult ecdysis. We show that its downregulation alters Burs expression in the CCAP neurons. Ectopic expression of Opa, or the vertebrate homologue Zic2 , in the CCAP neurons also affects Burs expression, indicating an evolutionary functional conservation. Finally, our results show that, independently of its role in Burs regulation, Opa prevents death of CCAP neurons during larval development.


Development ◽  
1997 ◽  
Vol 124 (24) ◽  
pp. 5021-5032 ◽  
Author(s):  
J.A. Cygan ◽  
R.L. Johnson ◽  
A.P. McMahon

Classical embryological experiments have demonstrated that dorsal-ventral patterning of the vertebrate limb is dependent upon ectodermal signals. One such factor is Wnt-7a, a member of the Wnt family of secreted proteins, which is expressed in the dorsal ectoderm. Loss of Wnt-7a results in the appearance of ventral characteristics in the dorsal half of the distal limb. Conversely, En-1, a homeodomain transcription factor, is expressed exclusively in the ventral ectoderm, where it represses Wnt-7a. En-1 mutants have dorsal characteristics in the ventral half of the distal limb. Experiments in the chick suggest that the dorsalizing activity of Wnt-7a in the mesenchyme is mediated through the regulation of the LIM-homeodomain transcription factor Lmx-1. Here we have examined the relationship between Wnt-7a, En-1 and Lmx-1b, a mouse homolog of chick Lmx-1, in patterning the mammalian limb. We find that Wnt-7a is required for Lmx-1b expression in distal limb mesenchyme, and that Lmx-1b activation in the ventral mesenchyme of En-1 mutants requires Wnt-7a. Consistent with Lmx-1b playing a primary role in dorsalization of the limb, we find a direct correlation between regions of the anterior distal limb in which Lmx-lb is misregulated during limb development and the localization of dorsal-ventral patterning defects in Wnt-7a and En-1 mutant adults. Thus, ectopic Wnt-7a expression and Lmx-1b activation underlie the dorsalized En-1 phenotype, although our analysis also reveals a Wnt-7a-independent activity for En-1 in the repression of pigmentation in the ventral epidermis. Finally, we demonstrate that ectopic expression of Wnt-7a in the ventral limb ectoderm of En-1 mutants results in the formation of a second, ventral apical ectodermal ridge (AER) at the junction between Wnt-7a-expressing and nonexpressing ectoderm. Unlike the normal AER, ectopic AER formation is dependent upon Wnt-7a activity, indicating that distinct genetic mechanisms may be involved in primary and secondary AER formation.


2008 ◽  
Vol 44 (3) ◽  
pp. 260-265
Author(s):  
D. V. Kopytova ◽  
M. R. Kopantseva ◽  
E. N. Nabirochkina ◽  
N. E. Vorobyova ◽  
S. G. Georgieva ◽  
...  

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Albert Tsai ◽  
Mariana RP Alves ◽  
Justin Crocker

We previously showed in Drosophila melanogaster embryos that low-affinity Ultrabithorax (Ubx)-responsive shavenbaby (svb) enhancers drive expression using localized transcriptional environments and that active svb enhancers on different chromosomes tended to colocalize (Tsai et al., 2017). Here, we test the hypothesis that these multi-enhancer ‘hubs’ improve phenotypic resilience to stress by buffering against decreases in transcription factor concentrations and transcriptional output. Deleting a redundant enhancer from the svb locus led to reduced trichome numbers in embryos raised at elevated temperatures. Using high-resolution fluorescence microscopy, we observed lower Ubx concentration and transcriptional output in this deletion allele. Transcription sites of the full svb cis-regulatory region inserted into a different chromosome colocalized with the svb locus, increasing Ubx concentration, the transcriptional output of svb, and partially rescuing the phenotype. Thus, multiple enhancers could reinforce a local transcriptional hub to buffer against environmental stresses and genetic perturbations, providing a mechanism for phenotypical robustness.


Genome ◽  
1989 ◽  
Vol 31 (2) ◽  
pp. 677-683 ◽  
Author(s):  
S. C. Lakhotia

The 93D locus in Drosophila melanogaster and the 93D-like loci in other species of Drosophila, collectively termed hsr ω (heat shock RNA omega) locus, display several unique and intriguing features: (i) developmental regulation and selective induction by several agents like benzamide, colchicine, thiamphenicol, vit-B6; (ii) functional conservation in the genus but a very rapid DNA base sequence divergence; (iii) in spite of the rapid DNA sequence divergence, a strong conservation of organization (a 5′ unique region and a 3′ long tandem repeat region) and the pattern of multiple ω transcripts in the genus; (iv) a general nontranslatability of all the three major species of ω transcripts (an ~ 10-kb ω1, a 2.0-kb ω2, and a 1.2-kb ω3 species) although some recent evidence favours translatability of a small open reading frame (~ 23 – 27 amino acid long) in the ω3 transcript; (v) dispensability of the hsr ω locus for heat shock protein synthesis but indispensability for viability of flies. The heat shock inducibility of the 93D locus of D. melanogaster is selectively repressed by (i) combination of heat shock with another inducer of 93D; (ii) rearing of larvae at 10 °C; (iii) heterozygous deficiency for the 93D region; and (iv) conditions that alter levels of beta-alanine. In all cases of repression of the 93D locus during heat shock, the 87A and 87C loci (the two duplicate loci harbouring multiple copies for hsp70 and the alpha–beta repeat sequences (at 87C)) develop unequal puffs. The hsr ω locus appears to be under a complex system of regulation involving autoregulation as well as regulation by other factors in the cell which possibly operate through different control elements on the locus.Key words: benzamide, colchicine, beta-alanine, hsr ω, heat shock puffs, Drosophila.


Development ◽  
2000 ◽  
Vol 127 (19) ◽  
pp. 4169-4178 ◽  
Author(s):  
H. Grandel ◽  
B.W. Draper ◽  
S. Schulte-Merker

Classical embryological studies have implied the existence of an apical ectodermal maintenance factor (AEMF) that sustains signaling from the apical ectodermal ridge (AER) during vertebrate limb development. Recent evidence suggests that AEMF activity is composed of different signals involving both a sonic hedgehog (Shh) signal and a fibroblast growth factor 10 (Fgf10) signal from the mesenchyme. In this study we show that the product of the dackel (dak) gene is one of the components that acts in the epidermis of the zebrafish pectoral fin bud to maintain signaling from the apical fold, which is homologous to the AER of tetrapods. dak acts synergistically with Shh to induce fgf4 and fgf8 expression but independently of Shh in promoting apical fold morphogenesis. The failure of dak mutant fin buds to progress from the initial fin induction phase to the autonomous outgrowth phase causes loss of both AER and Shh activity, and subsequently results in a proximodistal truncation of the fin, similar to the result obtained by ridge ablation experiments in the chicken. Further analysis of the dak mutant phenotype indicates that the activity of the transcription factor engrailed 1 (En1) in the ventral non-ridge ectoderm also depends on a maintenance signal probably provided by the ridge. This result uncovers a new interaction between the AER and the dorsoventral organizer in the zebrafish pectoral fin bud.


2020 ◽  
Vol 40 (12) ◽  
Author(s):  
Mun Kyoung Kim ◽  
An Tranvo ◽  
Ann Marie Hurlburt ◽  
Neha Verma ◽  
Phuc Phan ◽  
...  

ABSTRACT U6 snRNA is transcribed by RNA polymerase III (Pol III) and has an external upstream promoter that consists of a TATA sequence recognized by the TBP subunit of the Pol III basal transcription factor IIIB and a proximal sequence element (PSE) recognized by the small nuclear RNA activating protein complex (SNAPc). Previously, we found that Drosophila melanogaster SNAPc (DmSNAPc) bound to the U6 PSE can recruit the Pol III general transcription factor Bdp1 to form a stable complex with the DNA. Here, we show that DmSNAPc-Bdp1 can recruit TBP to the U6 promoter, and we identify a region of Bdp1 that is sufficient for TBP recruitment. Moreover, we find that this same region of Bdp1 cross-links to nucleotides within the U6 PSE at positions that also cross-link to DmSNAPc. Finally, cross-linking mass spectrometry reveals likely interactions of specific DmSNAPc subunits with Bdp1 and TBP. These data, together with previous findings, have allowed us to build a more comprehensive model of the DmSNAPc-Bdp1-TBP complex on the U6 promoter that includes nearly all of DmSNAPc, a portion of Bdp1, and the conserved region of TBP.


Cell Reports ◽  
2019 ◽  
Vol 27 (3) ◽  
pp. 955-970.e7 ◽  
Author(s):  
Leila Shokri ◽  
Sachi Inukai ◽  
Antonina Hafner ◽  
Kathryn Weinand ◽  
Korneel Hens ◽  
...  

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