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Genetic and molecular analysis of ot...

Solomon, Keely Suzanne.

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Genetic and molecular analysis of otic placode formation in Danio rerio.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Genetic and molecular analysis of otic placode formation in Danio rerio./
作者:	Solomon, Keely Suzanne.
面頁冊數:	275 p.
附註:	Adviser: Andreas Fritz.
Contained By:	Dissertation Abstracts International64-02B.
標題:	Biology, Animal Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3080362

Genetic and molecular analysis of otic placode formation in Danio rerio.
Solomon, Keely Suzanne.

Genetic and molecular analysis of otic placode formation in Danio rerio. - 275 p.

Adviser: Andreas Fritz.

Thesis (Ph.D.)--Emory University, 2003.

Vertebrate cranial sensory organs and ganglia are derived from sensory placodes, which develop as thickenings of ectoderm at the lateral border of the neural plate during late gastrulation to early neurulation in most species. The otic placode gives rise to the inner ear, a complex sensory structure responsible for the detection of sound, gravity and acceleration. Classical embryological grafting studies have demonstrated that formation of the otic placode is a complex, multistep process requiring interactions between multiple tissues. More recent analyses have identified several members of the fibroblast growth factor (Fgf) family of molecules as key inductive signals required for this process. However, comparatively little is known about the early molecular players that function within the otic precursor domain to mediate these inductive signals.Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Genetic and molecular analysis of otic placode formation in Danio rerio.
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035 $a (UnM)AAI3080362
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100 1 $a Solomon, Keely Suzanne. $3 1258436
245 1 0 $a Genetic and molecular analysis of otic placode formation in Danio rerio.
300 $a 275 p.
500 $a Adviser: Andreas Fritz.
500 $a Source: Dissertation Abstracts International, Volume: 64-02, Section: B, page: 0529.
502 $a Thesis (Ph.D.)--Emory University, 2003.
520 $a Vertebrate cranial sensory organs and ganglia are derived from sensory placodes, which develop as thickenings of ectoderm at the lateral border of the neural plate during late gastrulation to early neurulation in most species. The otic placode gives rise to the inner ear, a complex sensory structure responsible for the detection of sound, gravity and acceleration. Classical embryological grafting studies have demonstrated that formation of the otic placode is a complex, multistep process requiring interactions between multiple tissues. More recent analyses have identified several members of the fibroblast growth factor (Fgf) family of molecules as key inductive signals required for this process. However, comparatively little is known about the early molecular players that function within the otic precursor domain to mediate these inductive signals.
520 $a In my dissertation work, I have identified the <italic>hearsay</italic> mutation, which leads to a defect in the initiation of otic placode formation. My analysis reveals that this mutation is caused by a disruption of the zebrafish forkhead domain-containing transcription factor <italic>foxi1</italic>, which is expressed within the presumptive otic anlagen throughout gastrulation. Expression of <italic>pax8</italic>, the earliest known marker for the otic primordia, is absent in these mutants, and misexpression of <italic>foxi1 </italic> can induce ectopic expression of <italic>pax8</italic>. Therefore, <italic> foxi1</italic> may act as one of the first genes within the otic primordia to mediate inductive signals required for the formation of this tissue. I have also demonstrated an early, partially redundant function for <italic> Distal</italic>-<italic>less</italic> transcription factors <italic>dlx3b </italic> and <italic>dlx4b</italic> in otic placode formation. <italic>dlx3b </italic> and <italic>dlx4b</italic> are expressed within the otic primordia during late gastrulation, and loss of function for these genes leads to a reduction or loss of the otic placode. Expression of several early markers for the otic primordia is absent in these embryos, although <italic>pax8</italic> initiates normally, demonstrating a slightly later function than <italic> foxi1</italic>. Combined loss-of-function for <italic>foxi1/dlx3b/dlx4b</italic> leads to a strong, synergistic phenotype; otic placode formation is completely ablated in these embryos. Together, these analyses suggest a model for otic placode formation in which <italic>foxi1</italic> and <italic>dlx3b/4b</italic> function in parallel to mediate different temporal and/or spatial aspects of <italic>fgf3/8</italic> inductive signaling.
590 $a School code: 0665.
650 4 $a Biology, Animal Physiology. $3 1017835
650 4 $a Biology, Genetics. $3 1017730
650 4 $a Biology, Molecular. $3 1017719
690 $a 0307
690 $a 0369
690 $a 0433
710 2 0 $a Emory University. $3 1017429
773 0 $t Dissertation Abstracts International $g 64-02B.
790 $a 0665
790 1 0 $a Fritz, Andreas, $e advisor
791 $a Ph.D.
792 $a 2003
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3080362