Key to our understanding of growth regulation in Drosophila would be discovering a ligand that could regulate steroid synthesis. Activins are involved in regulating steroid hormone release in vertebrates. In invertebrates, they most likely function to keep ecdysone levels low to allow the larvae more time to achieve critical weight in order to initiate the metamorphic process. TGF-B(Transforming Growth Factor Beta) is a family of cytokine growth factors. We find that two members of the TGF-B signaling pathway Drosophila Activin (dACT) and Activin-like ligand Dawdle (DAW) signal through the type I receptor Baboon (BABO) and the type II receptor PUNT to primarily activate the transcription factor dSMAD2 and MAD to a lesser extent. One transcription factor brinker (brk) appears to be central to dACT signaling. / In wings dACT signaling is necessary to promote growth however, dACT is not expressed in wings suggesting that dACT is provided through the endocrine system. One possible target tissue of dACT signaling is the ring gland (RG), which synthesizes and secretes the steroid hormone ecdysone (E). Consistent with this idea, using the UAS/GAL-4 system, we find that over-expression of the TGF-B ligand dACT with the neuroendocrine driver 386Y-GAL4 results in an increase in the size of flies. Surprisingly, when we increase the dose with two copies of dACT, it decreases the size of flies also indicating non-autononomous effects. We find that overexpression of the activated form of the dACT type I receptor Baboon (BABO) or brk with the ring gland specific driver phm-GAL4 results in developmental arrest of larvae that stay small and never pupate. The developmental arrest can be overcome by feeding larvae E, suggesting that dACT represses E through brk. These results suggest a model where dACT signaling activates brk which inhibits E. We picked three cytochrome P450 enzymes: phantom (PHM), disembodied (DIS) and spookier (SPKR). / PHM is not regulated by any component in the dACT signaling pathway however, we find DIS and SPKR are down-regulated through brk. MAD and dSmad2 bind to a Smad binding site and MAD out-competes dSMAD2. We find no evidence that Drosophila insulin-like peptides (DILPS)/PI3- Kinase or Ras signal through the dActivin signaling pathway. / by Scott C. Gesualdi. / Thesis (Ph.D.)--Florida Atlantic University, 2009. / Includes bibliography. / Electronic reproduction. Boca Raton, Fla., 2009. Mode of access: World Wide Web.

Thesis (M. Sc.)--York University, 1999. Graduate Programme in Biology. / Typescript. Includes bibliographical references (leaves 88-96). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://wwwlib.umi.com/cr/yorku/fullcit?pMQ39222.

Smyd1 is the founder of a gene family whose members contain split SET and MYND Domains. Smyd1 has several SET dependent lysine methyl-transferase substrates, including multiple histone lysines and at least one non-histone protein, skNAC. The MYND domain of Smyd1 is required for protein interactions, such as that with skNAC. Conventional Smyd1 knockouts die at E10 due to cardiac defects, including an enrichment of cardiac jelly, a decrease in trabeculation, and the loss of ventricular septation. dHand, a transcription factor specific for right ventricular development, and Irx4, a ventricle specific gene, are down regulated. I have shown that an approximately one kb stretch of DNA sequence upstream of the muscle specific first exon of Smyd1 is sufficient to drive expression of a reporter in transgenic mice. Cardiac specific expression is mediated by a proximal Mef2 binding site whereas skeletal muscle expression is dependent on E-boxes. I have fully analyzed this stretch of sequence via computational methods and made predictions on other potential regulatory factors. Through the use of Cre mediated conditional knockouts, I have shown that the phenotype of the conventional knockout was not due to the introduction of the Neomycin cassette at the gene locus or due to cell non-autonomous effects on the heart. Smyd1 is not only essential for cardiac septation, but throughout embryonic cardiac development, during embryonic skeletal muscle development, and in adult cardiac tissue. Conditionally deficient Smyd1 embryonic hearts are less affected than conventional Smyd1 knockouts, but are embryonically lethal and show poor trabeculation, cardiac hemorrhaging, and a pericardial edema. I detail that the Nkx2.5-Cre mediated Smyd1 deletion phenocopies the skNAC conventional knockout and that both knockouts have similar changes in the expression levels of several genes. Furthermore, when Smyd1 is conditionally removed from adult cardiac tissue, survival rates are diminished. Surprisingly a skeletal muscle specific CKO of Smyd1 mediated by Myogenin-Cre has resulted in perinatal lethality, with a visible phenotype as early as E15. Evident in the phenotype is a large edema between the epithelium and skeletal muscle, fewer myoblasts, decreased muscle mass, increased degenerating cells, and a potentially defective differentiation process. / text

Reciprocal crosses between plants containing different genome numbers have been demonstrated to show alternate phenotypes in many species and are often lethal. The effects of interploidy crosses on kernel development in maize (Zea mays) have been reassessed using markers for two cell domains: the aleurone and the basal endosperm transfer layer (BETL); and by monitoring gene expression. The study confirms previous observations and offers novel insights into genomic interactions. Endosperms from maternal excess crosses (tetraploid mother, diploid father) displayed reduced mitotic activity, and an accelerated rate of differentiation generally, including early starch accumulation, and earlier, atypical aleurone formation. The BETL failed to form normally, being replaced with aleuronelike cells, except for a few interspersed cells. Gene expression was altered, including those encoding cell domain markers and storage molecules. Paternal excess endosperms (diploid mother, tetraploid father), showed an increase in cellular proliferation. Generally, differentiation was delayed: starch accumulation began late, and formation of the aleurone layer was delayed, and was morphologically highly irregular. BETL specification was also disturbed, with only a few cells showing characteristic wall modifications very late in development. Later development of the whole endosperm was characterized by ectopic gene expression, and zones of high cell proliferation. A greater proportion of the genome was mis-expressed in these crosses, reflecting the more extreme phenotype. Although expression levels of marker genes did not reflect the failure to develop a normal BETL, it may be that the cells in the BETL region had undergone an modified developmental program. This work is considered in the context of evolutionary models which state that different parental roles lead to differential expression of genes from their respective genomes, and is compared with evidence from arabidopsis. The current study is considered generally supportive of such models.

Thesis (Ph. D.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 194-230) Also available in print.

Thesis (Ph. D.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 194-230) Also available online.

Thesis (M. Phil.)--University of Hong Kong, 2005. / Title proper from title frame. Also available in printed format.

Thesis (Ph. D.)--McMaster University, 2003. / Advisor: Michael Rudnicki. Includes bibliographical references (leaves 187-228). Also available via World Wide Web.

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The C₄ photosynthetic cycle acts to concentrate CO₂ around the enzyme Rubisco. By doing so, C₄ photosynthesis leads to increased radiation, water and nitrogen use efficiencies. As such, C₄ photosynthesis is the most productive form of photosynthesis known. Because it enables such high levels of productivity there are large international efforts to introduce C₄ photosynthesis into non-C₄ crop species such as rice. Kranz anatomy is a characteristic leaf cellular arrangement of concentric rings of bundle sheath and mesophyll cells around closely spaced veins and is crucial to C₄ photosynthesis in almost all known examples. Despite the fact that Kranz has evolved on over 60 times independently little is known about the genetic regulation of Kranz development, as attempts to elucidate Kranz regulators using conventional mutagenesis screens have provided few insights. However, the advent of next generation DNA sequencing technologies has enabled the interrogation of genetic networks at a previously unprecedented scale. The work in this thesis describes a genome-wide transcriptomic analysis of leaf development in maize, a C₄ species, that develops both Kranz-type and non-Kranz-type leaves. Detailed bioinformatics analyses identified candidate regulators of both Kranz development and additional aspects of maize leaf development. Three of the identified Kranz candidates were functionally characterised in both C₄ and non-C₄ species. Furthermore, expression and phylogenetic analyses of GOLDEN2-LIKE (GLK) genes, a small transcription factor family previously implicated in C₄ development in maize, were extended to determine the generality of GLK function in C₄ evolution.