Potential Drosophila melanogaster fushi tarazu (ftz) regulators interacting with the ftz proximal enhancer.
Item
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Title
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Potential Drosophila melanogaster fushi tarazu (ftz) regulators interacting with the ftz proximal enhancer.
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Identifier
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AAI9908339
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identifier
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9908339
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Creator
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Landrigan, Mary Frances.
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Contributor
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Adviser: Leslie Pick
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Date
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1998
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Language
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English
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Publisher
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City University of New York.
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Subject
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Biology, Molecular
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Abstract
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fushi tarazu (ftz) is a homeobox-containing gene of the pair-rule class. ftz is expressed in seven stripes in the cellular blastoderm, and later in the nervous system. Mutation of this gene is lethal, resulting in the loss of every other parasegment. Control of ftz expression is at the level of transcription. The 5{dollar}\sp\prime{dollar} regulatory region of the gene has been subdivided into the zebra element, the neurogenic element, and the upstream element. The upstream element directs expression in stripes in the mesoderm and ectoderm in a distance- and orientation independent manner. The upstream element has been functionally partitioned into proximal and distal enhancer elements. The former directs reporter expression in seven mesodermal and ectodermal stripes. Nine protein binding sites have been identified in the proximal enhancer, and at least twelve separate proteins bind to these sites. Previously identified proteins which interact with these sites include Ftz protein, Ftz-F1, a Ftz cofactor, and Ttk, a putative ftz repressor. Two proteins which interact with site 2 are apparently unique to that site. Conditions which should allow the purification of these proteins were established but not fully implemented A possible third protein which interacted with this site was identified. Adf-1 is another previously recognized protein which was found to interact with multiple sites in the proximal enhancer. The gene encoding this factor was mutated by P element insertion into its coding region. Rescue by a P element containing the adf-1 coding region and flanking sequence was successful. Mutants of adf-1 fail to hatch, although the stage at which the mutation is lethal is not known. There is no effect of adf-1 mutation on ftz expression. ftz stripes are expressed normally, and ftz nervous system expression is unaffected in adf-1 mutants. ftz-lac Z reporter constructs are expressed normally. This suggests that the role of Adf-1 in the control of ftz is relatively minor.
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Type
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dissertation
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Source
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PQT Legacy CUNY.xlsx
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degree
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Ph.D.
