Spatial control of hairy protein expression during embryogenesis

Development ◽  
1989 ◽  
Vol 107 (3) ◽  
pp. 489-504 ◽  
Author(s):  
K.L. Hooper ◽  
S.M. Parkhurst ◽  
D. Ish-Horowicz
Keyword(s):  
Hierarchical Models ◽  
Polyclonal Antiserum ◽  
Wild Type ◽  
Spatial Cues ◽  
Protein Patterns ◽  
Pair Rule Gene ◽  
H Protein ◽  
Blastoderm Stage ◽  
Pair Rule ◽  
Phase Relationships

We have used a polyclonal antiserum specific for the Drosophila segmentation gene, hairy (h), to analyse its expression during embryogenesis. The pattern of wild-type expression resembles that of h transcription, being expressed in stripes at the blastoderm stage. h is also expressed later in the stomodaeum, proctodaeum, tracheal pits and mesoderm. We demonstrate that h protein stripes show consistent phase relationships to those of the even-skipped (eve) pair-rule gene. We examine h protein patterns in embryos mutant for other segmentation genes, including h itself. We show that lack of h activity appears not to affect h striping, arguing that h expression is not under autoregulatory control. We also show that h activity is not needed for tracheal invagination. Mutations that are rearranged upstream of the h gene cause the loss of specific stripes, indicating that the h promoter includes activating elements that respond to specific spatial cues. Our observations suggest that pair-rule striping may be under redundant control, and we discuss possible implications for hierarchical models of pair-rule gene action.

The zygotic control of Drosophila pair-rule gene expression. I. A search for new pair-rule regulatory loci

Development ◽  
1989 ◽  
Vol 107 (3) ◽  
pp. 663-672 ◽  
Author(s):  
S.H. Vavra ◽  
S.B. Carroll
Keyword(s):  
Gene Expression ◽  
Regulatory System ◽  
Wild Type ◽  
Periodic Patterns ◽  
Pair Rule Gene ◽  
New Type ◽  
Regulatory Loci ◽  
Direct Inspection ◽  
Pair Rule ◽  
Zygotic Control

The examination of pair-rule gene expression in wild-type and segmentation mutant embryos has identified many, but not necessarily all, of the elements of the regulatory system that establish their periodic patterns. Here we have conducted a new type of search for previously unknown regulators of these genes by examining pair-rule gene expression in blastoderm embryos lacking parts of or entire chromosomes. This method has the advantage of direct inspection of abnormal pair-rule gene patterns without relying upon mutagenesis or interpretation of larval phenotypes for the identification of segmentation genes. From these experiments we conclude that: (i) most zygotically required regulators of the fushi tarazu (ftz), even-skipped (eve) and hairy (h) pair-rule genes have been identified, except for one or more loci we have uncovered on chromosome arm 2L; (ii) the repression of the ftz and eve genes in the anterior third of the embryo is under maternal, not zygotic control; and (iii) there are no general zygotically required activators of pair-rule gene expression. The results suggest that the molecular basis of pair-rule gene regulation can be pursued with greater confidence now that most key trans-acting factors are already in hand.

Drosophila hairy pair-rule gene regulates embryonic patterning outside its apparent stripe domains

Development ◽  
1993 ◽  
Vol 118 (1) ◽  
pp. 255-266 ◽  
Author(s):  
M. Lardelli ◽  
D. Ish-Horowicz
Keyword(s):  
Transcription Initiation ◽  
Transcriptional Regulators ◽  
Early Embryo ◽  
Embryonic Patterning ◽  
Gene Deletions ◽  
Head Development ◽  
Pair Rule Gene ◽  
Blastoderm Stage ◽  
Embryonic Viability ◽  
Pair Rule

The hairy (h) segmentation gene of Drosophila regulates segmental patterning of the early embryo, and is expressed in a set of anteroposterior stripes during the blastoderm stage. We have used a set of h gene deletions to study the h promoter and the developmental requirements for individual h stripes. The results confirm upstream regulation of h striping but indicate that expression in the anterodorsal head domain depends on sequences downstream of the two transcription initiation sites. Surprisingly, the two anterior-most h domains appear to be dispensable for head development and embryonic viability. One partial promoter deletion expresses ectopic h, leading to misexpression of other segmentation genes and embryonic pattern defects. We demonstrate that h affects patterning outside its apparent stripe domains, supporting a model in which primary pair-rule genes act as concentration-dependent transcriptional regulators, i.e. as local morphogens.

odd Oz: A novel Drosophila pair rule gene

Cell ◽  
1994 ◽  
Vol 77 (4) ◽  
pp. 587-598 ◽  
Author(s):  
Anna Levine ◽  
Ayelet Bashan-Ahrend ◽  
Ofra Budai-Hadrian ◽  
Devorah Gartenberg ◽  
Sophia Menasherow ◽  
...  
Keyword(s):  
Pair Rule Gene ◽  
Pair Rule

scholarly journals Aspergillus nidulans Protein O-Mannosyltransferases Play Roles in Cell Wall Integrity and Developmental Patterning

2009 ◽  
Vol 8 (10) ◽  
pp. 1475-1485 ◽  
Author(s):  
Thanyanuch Kriangkripipat ◽  
Michelle Momany
Keyword(s):  
Cell Wall ◽  
Aspergillus Nidulans ◽  
Double Mutant ◽  
Elevated Temperatures ◽  
Cell Wall Integrity ◽  
Wild Type ◽  
Spatial Cues ◽  
Developmental Patterning ◽  
In The Wild ◽  
Increased Sensitivity

ABSTRACT Protein O-mannosyltransferases (Pmts) initiate O-mannosyl glycan biosynthesis from Ser and Thr residues of target proteins. Fungal Pmts are divided into three subfamilies, Pmt1, -2, and -4. Aspergillus nidulans possesses a single representative of each Pmt subfamily, pmtA (subfamily 2), pmtB (subfamily 1), and pmtC (subfamily 4). In this work, we show that single Δpmt mutants are viable and have unique phenotypes and that the ΔpmtA ΔpmtB double mutant is the only viable double mutant. This makes A. nidulans the first fungus in which all members of individual Pmt subfamilies can be deleted without loss of viability. At elevated temperatures, all A. nidulans Δpmt mutants show cell wall-associated defects and increased sensitivity to cell wall-perturbing agents. The Δpmt mutants also show defects in developmental patterning. Germ tube emergence is early in ΔpmtA and more frequent in ΔpmtC mutants than in the wild type. In ΔpmtB mutants, intrahyphal hyphae develop. All Δpmt mutants show distinct conidiophore defects. The ΔpmtA strain has swollen vesicles and conidiogenous cells, the ΔpmtB strain has swollen conidiophore stalks, and the ΔpmtC strain has dramatically elongated conidiophore stalks. We also show that AN5660, an ortholog of Saccharomyces cerevisiae Wsc1p, is modified by PmtA and PmtC. The Δpmt phenotypes at elevated temperatures, increased sensitivity to cell wall-perturbing agents and restoration to wild-type growth with osmoticum suggest that A. nidulans Pmts modify proteins in the cell wall integrity pathway. The altered developmental patterns in Δpmt mutants suggest that A. nidulans Pmts modify proteins that serve as spatial cues.

Teneurin-1, a vertebrate homologue of the Drosophila pair-rule gene ten-m, is a neuronal protein with a novel type of heparin-binding domain

1999 ◽  
Vol 112 (12) ◽  
pp. 2019-2032 ◽  
Author(s):  
A.D. Minet ◽  
B.P. Rubin ◽  
R.P. Tucker ◽  
S. Baumgartner ◽  
R. Chiquet-Ehrismann
Keyword(s):  
Sequence Motifs ◽  
Heparin Binding ◽  
Terminal Part ◽  
Phylogenetic Conservation ◽  
Neuronal Protein ◽  
Repeat Proteins ◽  
Heparin Binding Domain ◽  
Pair Rule Gene ◽  
Pair Rule

The Drosophila gene ten-m is the first pair-rule gene not encoding a transcription factor, but an extracellular protein. We have characterized a highly conserved chicken homologue that we call teneurin-1. The C-terminal part harbors 26 repetitive sequence motifs termed YD-repeats. The YD-repeats are most similar to the core of the rhs elements of Escherichia coli. Related repeats in toxin A of Clostridium difficile are known to bind specific carbohydrates. We show that recombinantly expressed proteins containing the YD-repeats of teneurin-1 bind to heparin. Furthermore, heparin lyase treatment of extracts of cells expressing recombinant YD-repeat protein releases this protein from high molecular mass aggregates. In situ hybridization and immunostaining reveals teneurin-1 expression in neurons of the developing visual system of chicken and Drosophila. This phylogenetic conservation of neuronal expression from flies to birds implies fundamental roles for teneurin-1 in neurogenesis. This is supported by the neurite outgrowth occurring on substrates made of recombinant YD-repeat proteins, which can be inhibited by heparin. Database searches resulted in the identification of ESTs encoding at least three further members of the teneurin family of proteins. Furthermore, the human teneurin-1 gene could be identified on chromosome Xq24/25, a region implied in an X-linked mental retardation syndrome.

scholarly journals Tc-knirps plays different roles in the specification of antennal and mandibular parasegment boundaries and is regulated by a pair-rule gene in the beetle Tribolium castaneum

2013 ◽  
Vol 13 (1) ◽  
pp. 25 ◽  
Author(s):  
Andrew D Peel ◽  
Julia Schanda ◽  
Daniela Grossmann ◽  
Frank Ruge ◽  
Georg Oberhofer ◽  
...  
Keyword(s):  
Tribolium Castaneum ◽  
Pair Rule Gene ◽  
Pair Rule

scholarly journals Unipolar distributions of junctional Myosin II identify cell stripe boundaries that drive cell intercalation throughout Drosophila axis extension

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Robert J Tetley ◽  
Guy B Blanchard ◽  
Alexander G Fletcher ◽  
Richard J Adams ◽  
Bénédicte Sanson
Keyword(s):  
Myosin Ii ◽  
Interaction Model ◽  
Cell Interaction ◽  
Cell Number ◽  
Cell Polarization ◽  
Convergence And Extension ◽  
Pair Rule Gene ◽  
Cell Intercalation ◽  
Pair Rule ◽  
Cell Cell

Convergence and extension movements elongate tissues during development. Drosophila germ-band extension (GBE) is one example, which requires active cell rearrangements driven by Myosin II planar polarisation. Here, we develop novel computational methods to analyse the spatiotemporal dynamics of Myosin II during GBE, at the scale of the tissue. We show that initial Myosin II bipolar cell polarization gives way to unipolar enrichment at parasegmental boundaries and two further boundaries within each parasegment, concomitant with a doubling of cell number as the tissue elongates. These boundaries are the primary sites of cell intercalation, behaving as mechanical barriers and providing a mechanism for how cells remain ordered during GBE. Enrichment at parasegment boundaries during GBE is independent of Wingless signaling, suggesting pair-rule gene control. Our results are consistent with recent work showing that a combinatorial code of Toll-like receptors downstream of pair-rule genes contributes to Myosin II polarization via local cell-cell interactions. We propose an updated cell-cell interaction model for Myosin II polarization that we tested in a vertex-based simulation.

scholarly journals The temporal transcription factor E93 controls dynamic enhancer activity and chromatin accessibility during development

2019 ◽  
Author(s):  
Spencer L. Nystrom ◽  
Matthew J. Niederhuber ◽  
Daniel J. McKay
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Developmental Time ◽  
Chromatin Accessibility ◽  
Wild Type ◽  
Spatial Cues ◽  
Enhancer Activity ◽  
Temporal Gene Expression ◽  
Developmental Program ◽  
Temporal Cues

ABSTRACTHow temporal cues combine with spatial inputs to control gene expression during development is poorly understood. Here, we test the hypothesis that the Drosophila transcription factor E93 controls temporal gene expression by regulating chromatin accessibility. Precocious expression of E93 early in wing development reveals that it can simultaneously activate and deactivate different target enhancers. Notably, the precocious patterns of enhancer activity resemble the wild-type patterns that occur later in development, suggesting that provision of E93 alters the competence of enhancers to respond to spatial cues. Genomic profiling reveals that precocious E93 expression is sufficient to regulate chromatin accessibility at a subset of its targets. These accessibility changes mimic those that normally occur later in development, indicating that precocious E93 accelerates the wild-type developmental program. Further, we find that target enhancers that do not respond to precocious E93 in early wings become responsive after a developmental transition, suggesting that parallel temporal pathways work alongside E93. These findings support a model wherein E93 expression functions as an instructive cue that defines a broad window of developmental time through control of chromatin accessibility.

scholarly journals Odd-paired controls frequency doubling in Drosophila segmentation by altering the pair-rule gene regulatory network

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Erik Clark ◽  
Michael Akam
Keyword(s):  
Gene Expression ◽  
Gene Regulatory Network ◽  
Regulatory Network ◽  
Frequency Doubling ◽  
Drosophila Embryo ◽  
Anteroposterior Patterning ◽  
Regulatory Interactions ◽  
Pair Rule Gene ◽  
Gene Regulatory ◽  
Pair Rule

The Drosophila embryo transiently exhibits a double-segment periodicity, defined by the expression of seven 'pair-rule' genes, each in a pattern of seven stripes. At gastrulation, interactions between the pair-rule genes lead to frequency doubling and the patterning of 14 parasegment boundaries. In contrast to earlier stages of Drosophila anteroposterior patterning, this transition is not well understood. By carefully analysing the spatiotemporal dynamics of pair-rule gene expression, we demonstrate that frequency-doubling is precipitated by multiple coordinated changes to the network of regulatory interactions between the pair-rule genes. We identify the broadly expressed but temporally patterned transcription factor, Odd-paired (Opa/Zic), as the cause of these changes, and show that the patterning of the even-numbered parasegment boundaries relies on Opa-dependent regulatory interactions. Our findings indicate that the pair-rule gene regulatory network has a temporally modulated topology, permitting the pair-rule genes to play stage-specific patterning roles.

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