Ecdysone receptor (EcR) regulates cell migration and chorion gene amplification in the Drosophila ovary. Jennifer Faye Hackney

ISBN: 9780549612537

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NOOKstudy eTextbook

148 pages


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Ecdysone receptor (EcR) regulates cell migration and chorion gene amplification in the Drosophila ovary.  by  Jennifer Faye Hackney

Ecdysone receptor (EcR) regulates cell migration and chorion gene amplification in the Drosophila ovary. by Jennifer Faye Hackney
| NOOKstudy eTextbook | PDF, EPUB, FB2, DjVu, talking book, mp3, ZIP | 148 pages | ISBN: 9780549612537 | 4.14 Mb

Ecdysone Receptor (EcR) mediates effects of the hormone ecdysone during larval molts, pupal metamorphosis, and adult female oogenesis. In the ovary, egg chamber formation requires interactions between the somatic follicle cell (FC) epithelium and theMoreEcdysone Receptor (EcR) mediates effects of the hormone ecdysone during larval molts, pupal metamorphosis, and adult female oogenesis.

In the ovary, egg chamber formation requires interactions between the somatic follicle cell (FC) epithelium and the germ line nurse cell/oocyte cyst. Previous work has shown EcR is required in the germ line for egg chamber maturation, and here I examine EcR requirements in the FC at late stages of oogenesis. EcR protein is ubiquitous in the FC but its activity is restricted to specific FC subsets, visualized by activity of an GAL4-EcR ligand sensor. GAL4-EcR is sensitive to an ecdysone agonist in organ culture and repressed in vivo by Ras GTPase signaling.

To determine the significance of restricted sites of EcR activity in the FC, I used targeted misexpression of dominant negative EcR (EcR-DN) molecules which resulted in (1) abnormal FC migrations, including aberrant centripetal migration and dorsal appendage tube formation, (2) increases in DE-cadherin expression and abnormal epithelial junction formation and (3) thin eggshell phenotypes that correlated with both reduced levels of chorion gene expression and reduction in chorion gene amplification.-Further investigation revealed two separable requirements for EcR in chorion gene amplification.

At stages 7-10A, both Flp-out misexpression of EcR-DN and mutant clones of a null allele in usp, which encodes the RXR partner of EcR, result in precocious amplification of the chorion genes, as measured by ectopic incorporation of BrdU. This indicates that EcR represses chorion gene amplification prior to stage 10B. At later stages, usp null and EcR-DN clones do not incorporate BrdU, consistent with my observations that EcR is required for late chorion loci amplification.

Consistent with a direct role in chorion gene amplification, ChIP analysis reveals that EcR binds at or near ACE3 (Amplification Control Element on 3), which is required for amplification to occur.-Results shown here indicate that (1) tissue-specific modulation of EcR activity by the Ras signaling pathway refines temporal ecdysone signals that regulate FC differentiation and cadherin-mediated epithelial cell shape changes and (2) EcR/USP bind to chorion gene cis-acting DNA elements to mediate a hormonal signal that triggers gene amplification.



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