Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Molecular influences relating to the development and biomineralization of the chiton radula, Acanthopleura histosa

ABSTRACT: Chitons are marine molluscs that posses a radula, a tongue like appendage containing many rows of microscopic teeth used for feeding. These teeth are hardened through the incorporation of biominerals. Since the original discovery of iron oxide and magnetite in these teeth, a wealth of chemical and structural knowledge has accumulated. The biomineralization process is known to be matrix mediated with precise control of the deposition of a number of different iron and calcium minerals at readily identifiable stages of tooth development. While much is known about the mechanisms of tooth mineralisation, there have been no studies undertaken to identify the genes that regulate this process. This investigation uses microarray technology to analyse the spatial expression of 493 expressed sequence tags (EST) derived from the radula sac of chiton, Acanthopleura hirtosa. A number of ESTs have been deemed significantly differentially expressed in relation to three designated areas of the radula sac. These spatial sections are defined by the variation in biomineral deposits of the radula, being immature radula which lacks any biomineral incorporation, iron deposition and calcium deposition. Additionally, foot muscle was used as a control to specify whether EST expression was specific to the radula and therefore likely involved biomineralization. A total of twelve A. hirtosa specimens were collected and sacrificed for microarray hybridizations. The radulae were removed from each animal immediately following sacrifice and dissected into three sections based on the biomineralisation development of the radula teeth. These sections are termed immature teeth, iron deposited teeth, and calcium deposited teeth. An additional sample of A. hirtosa foot muscle was taken from each specimen. RNA was extracted individually from these sections. Extracted RNA samples across subjects were pooled equally within sections in order to minimize the impact of biological variation and maximize the number of individual samples included in the study. To this effect, four single channel hybridizations were conducted for each radula and muscle section each representing a pooled biological replicate containing equal proportions of RNA from three A. hirtosa individuals. A total of sixteen microarray hybridizations were conducted in this manner.

ORGANISM(S): Acanthopleura hirtosa

SUBMITTER: Luke Gardner

PROVIDER: E-GEOD-20105 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:The signaling cascades that direct the morphological differentiation of the vascular system during early embryogenesis are not well defined. To further understand the role of Notch signaling during endothelial differentiation, this study uses both an in vivo gain-of-function and in vivo loss-of-function approach. At embryonic day 9.5, embryos with activated Notch1 signaling in the endothelia display a variety of growth and cardiovascular defects, and die soon after E10.5. Most notably, the extra-embryonic vasculature of the yolk sac displays remodeling differentiation defects. In the wild-type yolk sac, the primary vascular network has begun to reorganize, forming the large primary vessels and the smaller capillaries. In the activated Notch1 embryos remodeling is defective; the vasculature have an enlarged surface with decreased inter-vessel space. Embryos with ablated Notch signaling also display growth and vascular defects at E9.5 similar to the activated Notch1 embryos, however they exhibit a lack of vascular remodeling in the yolk sac, retaining the simple vascular plexus seen at E8.5. These results indicate that Notch signaling plays a critical role in the remodeling of the vasculature in the early embryo, particularly in the extra embryonic region. A conditional transgenic system was used in this study to activate Notch signaling. The ubiquitous ROSA26Notch transgene with a Neo/stop cassette flanked by loxP sites, followed by the N1-ICD cDNA, was recombined with a Tie2-CRE mouse, resulting in the removal of the STOP cassette and the subsequent activation of the Notch1-intracellular domain. This allowed for the overexpression and expansion of Notch signaling in all endothelial cells. Male Tie2-Cre mice were mated with female ROSA26Notch mice and resulting embryos were dissected at embryonic day 9.5. To ablate Notch signaling, Tie2-Cre mice were used in a two generation cross to obtain Tie2-Cre; Rbpj flox/flox embryos. These embryos lack RBPJ binding activity in the endothelia. In both instances embryos were used for genotyping and the yolk sac were separated and used to isolate total RNA with an RNeasy mini kit. The RNA was analyzed with the Mouse Genome 430A Array from Affymetrix. Samples were performed in duplicate, and RNA from wild type yolk sac tissues was compared to activated Notch and RBPJ loss-of-function yolk sac tissues.

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Molecular influences relating to the development and biomineralization of the chiton radula, Acanthopleura histosa

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