RESUMO
In this study, Meyerozyma caribbica, an indigenously isolated oleaginous yeast, produced in media containing glucose a bioemulsifier that was partially characterized as a proteoglycan based on preliminary analysis. Optimization of carbon:nitrogen (C:N) ratio revealed 30:1 as the suitable ratio for enhanced production. Apart from higher emulsification activity (E24: 70-80%), this molecule showed strong emulsion stability over a wide range of pH (2.0-9.0), salinity (0.05%-10%, w/v) and temperature (- 80 °C to + 50 °C). The current study emphasizes on the determination of critical media parameters for improved and stable bioemulsifier production coupled with partial characterization and identification of the molecule. Thus, a proteoglycan-based bioemulsifier with such a stable emulsifying property can serve as a versatile and potential component in food, cosmetics and pharmaceutical formulations.
Assuntos
Emulsificantes , Proteínas Fúngicas , Proteoglicanas , Saccharomycetales/metabolismo , Emulsificantes/química , Emulsificantes/isolamento & purificação , Proteínas Fúngicas/biossíntese , Proteínas Fúngicas/química , Proteínas Fúngicas/isolamento & purificação , Proteoglicanas/biossíntese , Proteoglicanas/química , Proteoglicanas/isolamento & purificaçãoRESUMO
Hox mediated neuroblast apoptosis is a prevalent way to pattern larval central nervous system (CNS) by different Hox genes, but the mechanism of this apoptosis is not understood. Our studies with Abdominal-A (Abd-A) mediated larval neuroblast (pNB) apoptosis suggests that AbdA, its cofactor Extradenticle (Exd), a helix-loop-helix transcription factor Grainyhead (Grh), and Notch signaling transcriptionally contribute to expression of RHG family of apoptotic genes. We find that Grh, AbdA, and Exd function together at multiple motifs on the apoptotic enhancer. In vivo mutagenesis of these motifs suggest that they are important for the maintenance of the activity of the enhancer rather than its initiation. We also find that Exd function is independent of its known partner homothorax in this apoptosis. We extend some of our findings to Deformed expressing region of sub-esophageal ganglia where pNBs undergo a similar Hox dependent apoptosis. We propose a mechanism where common players like Exd-Grh-Notch work with different Hox genes through region specific enhancers to pattern respective segments of larval central nervous system.
Assuntos
Apoptose/genética , Sistema Nervoso Central/crescimento & desenvolvimento , Proteínas de Ligação a DNA/metabolismo , Proteínas de Drosophila/metabolismo , Drosophila/genética , Proteínas de Homeodomínio/metabolismo , Receptores Notch/metabolismo , Fatores de Transcrição/metabolismo , Sequência de Aminoácidos , Animais , Proteínas de Ligação a DNA/genética , Drosophila/crescimento & desenvolvimento , Proteínas de Drosophila/genética , Elementos Facilitadores Genéticos , Feminino , Regulação da Expressão Gênica no Desenvolvimento , Genes Homeobox , Proteínas de Homeodomínio/genética , Larva/genética , Larva/crescimento & desenvolvimento , Masculino , Proteínas Nucleares/genética , Proteínas Nucleares/metabolismo , Receptores Notch/genética , Fatores de Transcrição/genéticaRESUMO
The expression and regulation of Hox genes in developing central nervous system (CNS) lack important details like specific cell types where Hox genes are expressed and the transcriptional regulatory players involved in these cells. In this study we have investigated the expression and regulation of Drosophila Hox gene Deformed (Dfd) in specific cell types of embryonic CNS. Using Dfd neural autoregulatory enhancer we find that Dfd autoregulates itself in cells of mandibular neuromere. We have also investigated the role of a Hox cofactor Homothorax (Hth) for its role in regulating Dfd expression in CNS. We find that Hth exhibits a region specific role in controlling the expression of Dfd, but has no direct role in mandibular Dfd neural autoregulatory circuit. Our results also suggest that homeodomain of Hth is not required for regulating Dfd expression in embryonic CNS.