Structural complexity and evolutionary conservation of the Drosophila homeotic gene proboscipedia.

Cribbs, David L.; Pultz, Mary Anne; Johnson, Delia; Mazzulla, M.; Kaufman, Thomas C.

doi:10.1002/j.1460-2075.1992.tb05188.x

Cited by 74 publications

(34 citation statements)

References 78 publications

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“…Primary antibodies were: mouse anti-Abd-B [1:5; Developmental Studies Hybridoma Bank (DSHB)], mouse anti-Ubx (1:20; DSHB), mouse antiAntp (8C11; DSHB), mouse anti-prospero (DSHB), mouse anti-d-CSP2 (1:200; DSHB), rat anti-Elav (1:50; DSHB), mouse anti-Repo (DSHB), rabbit anti-Exd (Mann and Abu-Shaar, 1996), guinea pig anti-Hth (GP52) (Ryoo and Mann, 1999), rat anti-Abd-A (from B. Gebelein, Cincinnati Children's Hospital Medical Center, OH, USA), rabbit anti-Scr (CLU395, 1:500) (Joshi et al, 2010), rabbit anti-Pb (e9, 1:100) (Cribbs et al, 1992), guinea pig anti-Dfd (1:200; from W. Mcginnis, University California, San Diego, CA, USA), guinea pig anti-Lab (1:50,000; from B. Olstein, Columbia University Medical Center, NY, USA), guinea pig anti-Deadpan (1:1000, from J. Skeath, Washington University in St Louis, MO, USA), guinea pig anti-Dll (Estella et al, 2008) and rabbit anti-myc (Molecular Probes). Secondary antibodies were: AlexaFluor488, AlexaFluor555 and AlexaFluor647 conjugates (Molecular Probes).…”

Section: Immunohistochemistrymentioning

confidence: 99%

Dual role for Hox genes and Hox co-factors in conferring leg motoneuron survival and identity in Drosophila

2013

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SUMMARYAdult Drosophila walk using six multi-jointed legs, each controlled by ~50 leg motoneurons (MNs). Although MNs have stereotyped morphologies, little is known about how they are specified. Here, we describe the function of Hox genes and homothorax (hth), which encodes a Hox co-factor, in Drosophila leg MN development. Removing either Hox or Hth function from a single neuroblast (NB) lineage results in MN apoptosis. A single Hox gene, Antennapedia (Antp), is primarily responsible for MN survival in all three thoracic segments. When cell death is blocked, partially penetrant axon branching errors are observed in Hox mutant MNs. When single MNs are mutant, errors in both dendritic and axon arborizations are observed. Our data also suggest that Antp levels in postmitotic MNs are important for specifying their identities. Thus, in addition to being essential for survival, Hox and hth are required to specify accurate MN morphologies in a level-dependent manner.

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Section: Immunohistochemistrymentioning

confidence: 99%

Dual role for Hox genes and Hox co-factors in conferring leg motoneuron survival and identity in Drosophila

2013

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“…The following primary antibodies were used: rabbit-anti-Asense (1:5000) (Brand et al, 1993) (kindly provided by N. Y. Yan), rabbit-anti-Castor (1:1000; kindly provided by W. Odenwald), mouse-anti-Dachshund (1:250) (Mardon et al, 1994) (Developmental Studies Hybridoma Bank), rabbit-antiDeadpan (1:300) (Bier et al, 1992) (kindly provided by H. Vässin), anti-DIG-AP (1:1000, Roche), rat-anti-Empty spiracles (1:1000) (Walldorf and Gehring, 1992) (kindly provided by U. Walldorf), rabbit-anti-Eyeless (1:1000; kindly provided by U. Walldorf), mouseanti-Fasciclin 2 (1D4, 1:15, Developmental Studies Hybridoma Bank), mouse-anti-β-Galactosidase (1:500, Promega), rabbit-anti-β-Galactosidase (1:2500, Cappel), rabbit-anti-Hunchback (1:1000, kindly provided by M. Gonzales-Gaitan), mouse-anti-Invected (4D9,1:4) (Patel et al, 1989) (Developmental Studies Hybridoma Bank), rabbit-anti-Klumpfuss (1:1000) (Yang et al, 1997) (kindly provided by X. Yang and B. Chia), rabbit anti-Labial (1:100) (Diederich et al, 1991) (kindly provided by T. Kaufman), mouse-antiLadybird (1:2) (Jagla et al, 1997) (kindly provided by K. Jagla), ratanti-Orthodenticle (1:20) (Wieschaus et al, 1992) (kindly provided by S. Leuzinger and H. Reichert), rabbit-anti-POU-domain1 (1:500) (Yeo et al, 1995) (kindly provided by X. Yang and B. Chia), rabbit antiProboscipedia (1:200) (Cribbs et al, 1992) (kindly provided by D. Cribbs), rabbit-anti-Runt (1:500) (Dormand and Brand, 1998) (kindly provided by E. Dormand and A. Brand), rat-anti-Sloppy paired (1:300) (Cadigan et al, 1994b) (kindly provided by W. Gehring) and rabbit-anti-Twin of eyeless (1:400; kindly provided by U. Walldorf).…”

Section: Antibodies and Immunohistochemistrymentioning

confidence: 99%

Molecular markers for identified neuroblasts in the developing brain ofDrosophila

2003

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The Drosophila brain develops from the procephalic neurogenic region of the ectoderm. About 100 neural precursor cells (neuroblasts)delaminate from this region on either side in a reproducible spatiotemporal pattern. We provide neuroblast maps from different stages of the early embryo(stages 9, 10 and 11, when the entire population of neuroblasts has formed),in which about 40 molecular markers representing the expression patterns of 34 different genes are linked to individual neuroblasts. In particular, we present a detailed description of the spatiotemporal patterns of expression in the procephalic neuroectoderm and in the neuroblast layer of the gap genes empty spiracles, hunchback, huckebein, sloppy paired 1 and tailless; the homeotic gene labial; the early eye genes dachshund, eyeless and twin of eyeless; and several other marker genes (including castor, pdm1, fasciclin 2, klumpfuss, ladybird,runt and unplugged). We show that based on the combination of genes expressed, each brain neuroblast acquires a unique identity, and that it is possible to follow the fate of individual neuroblasts through early neurogenesis. Furthermore, despite the highly derived patterns of expression in the procephalic segments, the co-expression of specific molecular markers discloses the existence of serially homologous neuroblasts in neuromeres of the ventral nerve cord and the brain. Taking into consideration that all brain neuroblasts are now assigned to particular neuromeres and individually identified by their unique gene expression, and that the genes found to be expressed are likely candidates for controlling the development of the respective neuroblasts, our data provide a basic framework for studying the mechanisms leading to pattern and cell diversity in the Drosophilabrain, and for addressing those mechanisms that make the brain different from the truncal CNS.

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“…The presence of a lab-class intron which interrupts the homeobox is an interesting feature of HLXB9 and is shared with other genes which have the Q'VK protein sequence conserved at this position. 10 The 6 bp deletion is located immediately C-terminal of exon 2 and alters the conserved Q'VK protein sequence but does not change the intron-exon splicing consensus sequence.…”

Section: European Journal Of Human Geneticsmentioning

confidence: 99%

Spectrum of mutations and genotype–phenotype analysis in Currarino syndrome

2001

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The triad of a presacral tumour, sacral agenesis and anorectal malformation constitutes the Currarino syndrome which is caused by dorsal-ventral patterning defects during embryonic development. The syndrome occurs in the majority of patients as an autosomal dominant trait associated with mutations in the homeobox gene HLXB9 which encodes the nuclear protein HB9. However, genotype ± phenotype analyses have been performed only in a few families and there are no reports about the specific impact of HLXB9 mutations on HB9 function. We performed a mutational analysis in 72 individuals from nine families with Currarino syndrome. We identified a total of five HLXB9 mutations, four novel and one known mutation, in four out of four families and one out of five sporadic cases. Highly variable phenotypes and a low penetrance with half of all carriers being clinically asymptomatic were found in three families, whereas affected members of one family showed almost identical phenotypes. However, an obvious genotype ± phenotype correlation was not found. While HLXB9 mutations were diagnosed in 23 patients, no mutation or microdeletion was detected in four sporadic patients with Currarino syndrome. The distribution pattern of here and previously reported HLXB9 mutations indicates mutational predilection sites within exon 1 and the homeobox. Furthermore, sequence homology to Drosophila homeobox genes suggest that some of these mutations located within the homeobox may alter the DNA-binding specificity of HB9 while those in sequences homologous to a recently identified NLS motif of the human homeobox gene PDX-1 may impair nuclear translocation of the mutated protein. European Journal of Human Genetics (2001) 9, 599 ± 605.

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Structural complexity and evolutionary conservation of the Drosophila homeotic gene proboscipedia.

Cited by 74 publications

References 78 publications

Dual role for Hox genes and Hox co-factors in conferring leg motoneuron survival and identity in Drosophila

Dual role for Hox genes and Hox co-factors in conferring leg motoneuron survival and identity in Drosophila

Molecular markers for identified neuroblasts in the developing brain ofDrosophila

Spectrum of mutations and genotype–phenotype analysis in Currarino syndrome

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