7C female sterile mutants fail to accumulate early eggshell proteins necessary for later chorion morphogenesis in Drosophila

Bauer, Beverly Jean; Waring, Gail L.

doi:10.1016/0012-1606(87)90171-0

Cited by 27 publications

(17 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…First, shark is required in the DA cells for proper DA-chorion deposition, a complex process regulated at many levels (reviewed by Waring, 2000). Mutations that disrupt chorion-gene amplification or chorion-protein synthesis result in thin, collapsed DAs and main-body eggshell (Bauer and Waring, 1987;Landis et al, 1997;Mohler and Carroll, 1984;Nilson and Schüpbach, 1998).…”

Section: Discussionmentioning

confidence: 99%

bullwinkleandsharkregulate dorsal-appendage morphogenesis inDrosophilaoogenesis

Tran

Berg

2003

Development

View full text Add to dashboard Cite

bullwinkle (bwk) regulates embryonic anteroposterior patterning and, through a novel germline-to-soma signal, morphogenesis of the eggshell dorsal appendages. We screened for dominant modifiers of the bullwinkle mooseantler eggshell phenotype and identified shark, which encodes an SH2-domain, ankyrin-repeat tyrosine kinase. At the onset of dorsal-appendage formation, shark is expressed in a punctate pattern in the squamous stretch cells overlying the nurse cells. Confocal microscopy with cell-type-specific markers demonstrates that the stretch cells act as a substrate for the migrating dorsal-appendage-forming cells and extend cellular projections towards them. Mosaic analyses reveal that shark is required in follicle cells for cell migration and chorion deposition. Proper shark RNA expression in the stretch cells requires bwkactivity, while restoration of shark expression in the stretch cells suppresses the bwk dorsal-appendage phenotype. These results suggest that shark plays an important downstream role in the bwk-signaling pathway. Candidate testing implicates Src42Ain a similar role, suggesting conservation with a vertebrate signaling pathway involving non-receptor tyrosine kinases.

show abstract

Section: Discussionmentioning

confidence: 99%

bullwinkleandsharkregulate dorsal-appendage morphogenesis inDrosophilaoogenesis

Tran

Berg

2003

Development

View full text Add to dashboard Cite

show abstract

“…To identify which of the eggs produced by mosaic females were derived from egg chambers with homozygous mutant follicle cell clones, we developed a marker that incorporates information about the follicle cell genotype into the phenotype of the eggshell. This marker is a transgene bearing a dominant-negative form of the defective chorion 1 (dec-1) gene, which is required in the follicle cells for eggshell integrity (Bauer and Waring, 1987;Hawley and Waring, 1988). The dominantnegative version, P [decDN], bears an engineered deletion within the dec-1 coding region that causes dominant female sterility and the production of dec-like collapsed eggs (Spangenberg and Waring, 2007).…”

Section: Research Article Development 136 (17)mentioning

confidence: 99%

Graded Egfr activity patterns theDrosophilaeggshell independently of autocrine feedback

et al. 2009

View full text Add to dashboard Cite

The pattern of the Drosophila eggshell is determined by the establishment of a complex and stereotyped pattern of cell fates in the follicular epithelium of the ovary. Localized activation of the Epidermal growth factor receptor (Egfr) is essential for this patterning. Modulation of Egfr pathway activity in time and space determines distinct fates at their appropriate locations, but the details of how Egfr signaling is regulated and how the profile of Egfr activity corresponds to cell fate remain unclear. Here we analyze the effect of loss of various Egfr regulators and targets on follicle cell patterning, using a marker for follicle cell fate, and on the mature eggshell phenotype, using a novel eggshell marker. We show, contrary to current patterning models, that feedback regulation of Egfr activity by the autocrine ligand Spitz and the inhibitor Argos is not necessary for patterning. Given the cell-autonomous nature of the mutant phenotypes we observed, we propose instead that the pattern of cell fates is generated by spatial information derived directly from the germline ligand Gurken, without a requirement for subsequent patterning by diffusible Egfr regulators in the follicular epithelium.

show abstract

“…The dec-1 ct4b1 deficiency chromosome and the dec-1 mutant alleles, dec-1 29 (fs(1)410) and dec-1 4 (fs(1)1501), have been described previously (Bauer and Waring 1987;Hawley and Waring 1988). The dominantly marked, multiply inverted balancer chromosomes CyO; TM3, Ser and TM3, Sb were used for manipulations of the transgenic lines.…”

Section: Methodsmentioning

confidence: 99%

“…Several vitelline membrane and endochorion structural components have been identified (Waring 2000). Protein null mutants for three major structural components, DEC-1, s36, and sV23 (Digan et al 1979;Bauer and Waring 1987;Savant and Waring 1989), have been recovered in genetic screens for sterile females. Assembly defects manifested at the morphological level are associated with the s36 and dec-1 mutants.…”

mentioning

confidence: 99%

“…Assembly defects manifested at the morphological level are associated with the s36 and dec-1 mutants. An organized tripartite endochorion fails to organize in the absence of s36 (Digan et al 1979) while the endochorion collapses into the underlying vitelline membrane in DEC-1 protein null mutants (Bauer and Waring 1987). The identification of regions and motifs within the sV23 and DEC-1 proteins that are essential for eggshell assembly and function have been the focus of recent studies (Badciong et al 2001;Mauzy-Melitz and Waring 2003;Manogaran and Waring 2004).…”

mentioning

confidence: 99%

See 1 more Smart Citation

A Mutant dec-1 Transgene Induces Dominant Female Sterility in Drosophila melanogaster

Spangenberg

Waring

2007

Genetics

View full text Add to dashboard Cite

The Drosophila dec-1 gene produces three proproteins required for female fertility and eggshell assembly. The three proproteins are distinguished by their C termini. Fc106, the most abundant proprotein, is cleaved within the vitelline membrane to three mature derivatives in a developmentally regulated manner. To define sequences within fc106 that are critical for its function, we created wild-type and mutant versions of an fc106 cDNA transgene. The functional consequences of the mutations were assessed in dec-1 4 , a female-sterile splicing mutant that does not produce the fc106 isoform. The fertility of dec-1 4 females was restored by the introduction of either a wild-type transgene or a transgene bearing a C-terminal deletion that included fc106-specific sequences. Surprisingly, the removal of internal coding sequences created an aberrant DEC-1 proprotein that induced female sterility when introduced into wildtype flies. Dominant female sterility was not associated with larger deletions that included the fc106 N terminus, suggesting that abnormal juxtaposition of N-and C-terminal sequences in the aberrant proprotein interfered with endogenous DEC-1 proteins. Changes in the fractionation behavior of the endogenous fc106 C-terminal derivative, s60, and morphological changes in the endochorion in response to expression of the aberrant proprotein support this interpretation.

show abstract

7C female sterile mutants fail to accumulate early eggshell proteins necessary for later chorion morphogenesis in Drosophila

Cited by 27 publications

References 29 publications

bullwinkleandsharkregulate dorsal-appendage morphogenesis inDrosophilaoogenesis

bullwinkleandsharkregulate dorsal-appendage morphogenesis inDrosophilaoogenesis

Graded Egfr activity patterns theDrosophilaeggshell independently of autocrine feedback

A Mutant dec-1 Transgene Induces Dominant Female Sterility in Drosophila melanogaster

Contact Info

Product

Resources

About