Maternal inheritance of transcripts from three<i>Drosophila src</i>-related genes

Wadsworth, Samuel C.; Madhavan, Kornath; Bilodeau-Wentworth, Diana

doi:10.1093/nar/13.6.2153

Cited by 33 publications

(24 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, even in embryos that were homozygous mutant for one of these three genes, heterozygosity for the two remaining genes did not lead to additive or synergistic increases in commissure defects (Table 3). Because in other experiments, Abl and trio behaved genetically as fra effectors (see below), the inability of fra to dominantly enhance Abl or trio loss-of-commissure defects, and the lack of transheterozygous interactions between fra, Abl and trio, may be due to the presence of maternally-contributed Abl and trio in the embryo (Bennett and Hoffmann, 1992;Liebl et al, 2000;Wadsworth et al, 1985). Another possibility is that heterozygosity for fra simply does not reduce the effective dose enough to enhance Abl or trio loss-of-commissure phenotypes.…”

Section: Df(1)np5/y;triomentioning

confidence: 96%

The Abelson tyrosine kinase, the Trio GEF and Enabled interact with the Netrin receptor Frazzled in Drosophila

et al. 2005

View full text Add to dashboard Cite

The attractive Netrin receptor Frazzled (Fra), and the signaling molecules Abelson tyrosine kinase (Abl), the guanine nucleotide-exchange factor Trio, and the Abl substrate Enabled (Ena), all regulate axon pathfinding at the Drosophila embryonic CNS midline. We detect genetic and/or physical interactions between Fra and these effector molecules that suggest that they act in concert to guide axons across the midline. Mutations in Abl and trio dominantly enhance fra and Netrin mutant CNS phenotypes, and fra;Abl and fra;trio double mutants display a dramatic loss of axons in a majority of commissures. Conversely, heterozygosity for ena reduces the severity of the CNS phenotype in fra, Netrin and trio,Abl mutants. Consistent with an in vivo role for these molecules as effectors of Fra signaling, heterozygosity for Abl, trio or ena reduces the number of axons that inappropriately cross the midline in embryos expressing the chimeric Robo-Fra receptor. Fra interacts physically with Abl and Trio in GST-pulldown assays and in co-immunoprecipitation experiments. In addition, tyrosine phosphorylation of Trio and Fra is elevated in S2 cells when Abl levels are increased. Together, these data suggest that Abl, Trio, Ena and Fra are integrated into a complex signaling network that regulates axon guidance at the CNS midline.

show abstract

Section: Df(1)np5/y;triomentioning

confidence: 96%

The Abelson tyrosine kinase, the Trio GEF and Enabled interact with the Netrin receptor Frazzled in Drosophila

et al. 2005

View full text Add to dashboard Cite

show abstract

“…In Drosophila, there are two src homologs, src42 (Src42A -FlyBase) and src64, and one Tec family kinase encoded by tec29 (Btk29A -FlyBase) (Takahashi et al, 1996;Katzen et al, 1990;Vincent et al, 1989;Gregory et al, 1987;Wadsworth et al, 1985;Simon et al, 1985;Simon et al, 1983). There is evidence that these genes play a role in cytoskeletal regulation.…”

Section: Introductionmentioning

confidence: 99%

src64andtec29are required for microfilament contraction duringDrosophilacellularization

2004

View full text Add to dashboard Cite

Formation of the Drosophila cellular blastoderm involves both membrane invagination and cytoskeletal regulation. Mutations in src64and tec29 reveal a novel role for these genes in controlling contraction of the actin-myosin microfilament ring during this process. Although membrane invagination still proceeds in mutant embryos, its depth is not uniform, and basal closure of the cells does not occur during late cellularization. Double-mutant analysis between scraps, a mutation in anillin that eliminates microfilament rings, and bottleneck suggests that microfilaments can still contract even though they are not organized into rings. However, the failure of rings to contract in the src64 bottleneck double mutant suggests that src64 is required for microfilament ring contraction even in the absence of Bottleneck protein. Our results suggest that src64-dependent microfilament ring contraction is resisted by Bottleneck to create tension and coordinate membrane invagination during early cellularization. The absence of Bottleneck during late cellularization allows src64-dependent microfilament ring constriction to drive basal closure.

show abstract

“…Hybridization and DNA sequence analyses have revealed that two of these genes, designated Dsrc and Dash, appear to be homologous to the vertebrate oncogenes src and abl, respectively (10,23). Transcripts from these genes are maternally inherited and are present on polyribosomes in preblastoderm embryos, indicating that they encode gene products active during early embryonic development (13,28). In addition, transcripts from Dsrc and Dash have been shown to be most abundant in embryos and pupae and to be present in lower amounts in larval and adult stages, except in adult ovarian tissue (23,26,28).…”

mentioning

confidence: 99%

“…Transcripts from these genes are maternally inherited and are present on polyribosomes in preblastoderm embryos, indicating that they encode gene products active during early embryonic development (13,28). In addition, transcripts from Dsrc and Dash have been shown to be most abundant in embryos and pupae and to be present in lower amounts in larval and adult stages, except in adult ovarian tissue (23,26,28). This pattern of expression correlates well with the periods of maximal cell division during Drosophila development and suggests, by analogy with vertebrate src family genes, that these genes may play a role in the regulation of cell proliferation.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Primary sequence and developmental expression of a novel Drosophila melanogaster src gene.

Gregory¹,

Kammermeyer²,

Vincent³

et al. 1987

Mol. Cell. Biol.

View full text Add to dashboard Cite

We have sequenced a cDNA clone for the Drosophila melanogaster gene Dsrc28C, a homolog of the vertebrate gene c-src. The cDNA contains a single open reading frame encoding a protein of 66 kilodaltons which contains features highly conserved within the src family of tyrosine protein kinases. Novel structural features of the Dsrc28C protein include a basic pl and a polyglycine domain near the amino terminus. Cell-free translation of in vitro-transcribed RNA yielded a protein of the predicted size which could be immunoprecipitated by anti-v-src antisera. RNA blot hybridization revealed that the gene is expressed predominantly during embryogenesis, in imaginal disks of third-instar larvae, and in adult females. In situ hybridization showed that expression in adult females is largely confined to nurse cells and developing oocytes.

show abstract

Maternal inheritance of transcripts from threeDrosophila src-related genes

Cited by 33 publications

References 41 publications

The Abelson tyrosine kinase, the Trio GEF and Enabled interact with the Netrin receptor Frazzled in Drosophila

The Abelson tyrosine kinase, the Trio GEF and Enabled interact with the Netrin receptor Frazzled in Drosophila

src64andtec29are required for microfilament contraction duringDrosophilacellularization

Primary sequence and developmental expression of a novel Drosophila melanogaster src gene.

Contact Info

Product

Resources

About