241 |
The genetic dissection of the fruitless gene's functions during embryogenesis in Drosophila melanogasterSong, Ho-Juhn 16 August 2001 (has links)
The fruitless (fru) gene in Drosophila melanogaster is a multifunctional
gene having sex-specific functions in the regulation of male sexual behavior and
sex-nonspecific functions affecting adult viability and external morphology. While
much attention has focused on fru's sex-specific roles, little is known about its sex-nonspecific
functions. The embryonic central nervous system (CNS) is a prime
model system in which to study the genetic control of axonal outgrowth and proper
CNS formation. I have examined fru's sex-nonspecific role in embryonic neural
development. fru transcripts and FRU proteins from sex-nonspecific promoters are
expressed beginning at the earliest stages of neurogenesis and subsequently in both
neurons and glia. In embryos that lack most or all fru function, Fasciclin II- and
BP102-positive axons appeared to defasciculate from their normal pathway and
fasciculate along aberrant neuronal pathways, suggesting that one of fru's sex-nonspecific
roles is to regulate axonal differentiation. I next examined whether the
loss of fru function in FRU-expressing neuronal precursors causes neuronal fate
change. Analysis of fru mutant embryos revealed a lack of Even-skipped (Eve)
staining in Eve-expressing neurons, ectopic Eve staining in non-Eve-expressing
neurons and mispositioned dorsal Eve-expressing neurons, which suggests that fru
functions to maintain neuronal identity rather than to specify neuronal fate. In fru
mutants these defects in axonal projections and in Eve staining were rescued by the
expression of specific fru transgenes.
To better understand fru's function in the formation of the embryonic CNS,
I dissected out fru's function in neuron and glia through a genetic interaction study.
fru genetically interacts in neurons with longitudinal lacking to make proper axonal
projections. In addition, fru might be in the same genetic pathway as roundabout
(robo), a repulsive guidance receptor, and commissureless, a downregulator of
Robo, to ensure proper axonal pathfinding. Surprisingly, fru interacts with
tramtrack and glial cells missing to repress neuronal differentiation in the lateral
glia and with single-minded for the development of midline glia. Taken together,
fru function is required for proper axonal pathfinding in neurons and for proper
development of lateral and midline glia. / Graduation date: 2002
|
242 |
Molecular and physiological aspects of maize embryo maturationWhite, Constance N. 13 January 1995 (has links)
Experiments were performed to assess regulatory factors governing maize
embryo maturation and vivipary. Both visual and molecular markers of embryo
development were used to examine the roles of the hormones abscisic acid (ABA)
and gibberellins (GAs), as well as water stress in governing transit from early
embryogeny to maturation-phase development. A differential screen identified
cDNAs whose expression is impaired in maize viviparous mutants which fail to
undergo maturation and instead precociously germinate. The cDNAs isolated in this
screen absolutely required both ABA and the Viviparousl (Vpl) gene product for
expression both in vivo and in vitro. Two novel clones were isolated: a maize
homologue of the wheat metallothionein gene E[subscript]c and a second clone which may
encode a novel seed storage protein of maize. In a separate screen, a maize cDNA
encoding a Lea group 3 protein was isolated. Like many maturation-associated
genes, maize Lea 3 was shown to ABA-inducible but is also expressed in response
to water stress in the absence of ABA or the Vp 1 gene.
We examined whether gibberellins might also be a factor modulating
precocious germination. Gibberellin inhibitors applied to cultured wildtype embryos
suppressed precocious germination and enhanced anthocyanin accumulation in a
developmentally specific manner. These behaviors mimicked the effect of ABA and
they were reversed by the addition of exogenous GA���. Vivipary in vivo resulting
from diminished ABA levels could be suppressed by either chemical or genetic
reduction of GA levels in immature kernels and resulted in desiccation-tolerant seed.
In contrast, reduction of endogenous gibberellins did not suppress vivipary of the
ABA-insensitive mutant vp1. Temporal analysis of gibberellin accumulation in
developing kernels revealed the accumulation of two bioactive species (GA��� and
GA���) during a developmental window just prior to peak ABA levels. It is suggested
that these species stimulate a developmental program leading to vivipary in the
absence of sufficient levels of ABA and that reduction of GA levels reestablishes a
hormone balance appropriate for suppression of germination and induction of
maturation in ABA-deficient kernels. The failure to suppress vivipary via reduction
of GA levels in the ABA-insensitive mutant vp1 suggests that the wildtype gene
product functions downstream of the sites of GA and ABA action in regulation of
maturation versus germination. / Graduation date: 1995
|
243 |
Development of the Mouse NotochordTamplin, Owen James 08 March 2011 (has links)
During development of the vertebrate embryo, a highly conserved tissue called the organizer forms during gastrulation, and is required for establishment of the basic body plan. In mouse, the organizer gives rise to the node and notochord, which are both transient signaling centres involved in patterning the body axes. The genetic regulation and morphogenesis of these tissues, particularly in the mouse, is not well understood. To follow the formation of these tissues we used time-lapse live imaging together with conventional cell lineage tracking. This showed that the notochord has distinct morphogenetic origins along the anterior-posterior axis: anterior head process forms by condensation of dispersed midline organizer cells; trunk forms by convergent extension of node cells; tail forms from posteriorly migrating node cells—this challenges the previously accepted model that tail notochord forms by node regression. We have also found there are distinct genetic requirements within these different regions. Previous mouse mutant analysis showed that conserved transcription factors Foxa2 and Noto are required for either all notochord regions or just tail notochord, respectively. We found a novel genetic interaction between the two demonstrated Foxa2 compensates for Noto specifically in the trunk notochord. Furthermore, we found Noto has a conserved role in regulating axial (notochord) versus paraxial (somite) cell fate. Therefore, we proposed there are three distinct regions within the mouse notochord, each with its own unique morphogenetic origins and genetic control. We have also conducted two microarray-based screens to identify novel gene expression patterns in the node and notochord. First, we compared Foxa2 mutant and wild type gastrula embryos. Second, we isolated notochord progenitors from early somite stage embryos. Extensive in situ hybridization screening based on both data sets revealed over 50 node and notochord expression patterns. Lastly, we screened Foxa2-bound chromatin regions near these notochord-specific genes using a transient zebrafish expression assay, and identified two novel notochord cis-regulatory modules. Together, we found a combination of classical genetics, embryology, and novel imaging techniques, has given us a better understanding of the morphogenesis and genetic regulation of pattern formation in the developing mouse embryo.
|
244 |
Development of the Mouse NotochordTamplin, Owen James 08 March 2011 (has links)
During development of the vertebrate embryo, a highly conserved tissue called the organizer forms during gastrulation, and is required for establishment of the basic body plan. In mouse, the organizer gives rise to the node and notochord, which are both transient signaling centres involved in patterning the body axes. The genetic regulation and morphogenesis of these tissues, particularly in the mouse, is not well understood. To follow the formation of these tissues we used time-lapse live imaging together with conventional cell lineage tracking. This showed that the notochord has distinct morphogenetic origins along the anterior-posterior axis: anterior head process forms by condensation of dispersed midline organizer cells; trunk forms by convergent extension of node cells; tail forms from posteriorly migrating node cells—this challenges the previously accepted model that tail notochord forms by node regression. We have also found there are distinct genetic requirements within these different regions. Previous mouse mutant analysis showed that conserved transcription factors Foxa2 and Noto are required for either all notochord regions or just tail notochord, respectively. We found a novel genetic interaction between the two demonstrated Foxa2 compensates for Noto specifically in the trunk notochord. Furthermore, we found Noto has a conserved role in regulating axial (notochord) versus paraxial (somite) cell fate. Therefore, we proposed there are three distinct regions within the mouse notochord, each with its own unique morphogenetic origins and genetic control. We have also conducted two microarray-based screens to identify novel gene expression patterns in the node and notochord. First, we compared Foxa2 mutant and wild type gastrula embryos. Second, we isolated notochord progenitors from early somite stage embryos. Extensive in situ hybridization screening based on both data sets revealed over 50 node and notochord expression patterns. Lastly, we screened Foxa2-bound chromatin regions near these notochord-specific genes using a transient zebrafish expression assay, and identified two novel notochord cis-regulatory modules. Together, we found a combination of classical genetics, embryology, and novel imaging techniques, has given us a better understanding of the morphogenesis and genetic regulation of pattern formation in the developing mouse embryo.
|
245 |
A study of embryotrophic mechanism of human oviductal cells on mouse embryo development in vitroXu, Jiasen. January 2000 (has links)
Thesis (Ph. D.)--University of Hong Kong, 2001. / Includes bibliographical references (leaves 182-211).
|
246 |
The early embryology of Thalassema mellita (Conn.)Torrey, John Cutler, January 1900 (has links)
Thesis (Ph. D.)--Columbia University. / Literature referred to: p. 236-242. Reprinted from Annals of the New York academy of sciences, October 1903, vol. XIV, no. 3.
|
247 |
Comparative and experimental analysis of precocious cell-lineage diversification in the embryonic dorsoventral axis of the gastropod Ilyanassa /Goulding, Morgan Ben, January 2001 (has links)
Thesis (Ph. D.)--University of Texas at Austin, 2001. / Vita. Includes bibliographical references (leaves 109-118). Available also in a digital version from Dissertation Abstracts.
|
248 |
An investigation on the conversion of C3 to embryotrophic iC3b in the human oviductal cell-mouse embryo co-culture systemTse, Pui-keung., 謝沛強. January 2006 (has links)
published_or_final_version / Medical Sciences / Master / Master of Medical Sciences
|
249 |
In vitro effect of oviductal embryotrophic factors on the gene expressions of preimplantation mouse embryos陳倩瑩, Chan, Sin-ying, Cindy. January 2003 (has links)
published_or_final_version / Medical Sciences / Master / Master of Medical Sciences
|
250 |
Identification and characterization of human oviductal cell derived embryotrophic factor 3Lee, Yin-lau., 李燕柳. January 2004 (has links)
published_or_final_version / abstract / toc / Obstetrics and Gynaecology / Doctoral / Doctor of Philosophy
|
Page generated in 0.0289 seconds