Morphology of the gastric mill teeth in dotillid crabs (Crustacea: Brachyura: Dotillidae) from Indonesia.

The gastric mill is a prominent structure in the digestive system of brachyuran crabs, consisting of a median tooth plate and a pair of lateral tooth plates. Among crab species that are deposit feeders, the morphology and size of the gastric mill teeth are correlated with the preferred substrate types and food spectrum. In this study, we provide a detailed description of the morphology of the median and lateral teeth of the gastric mills in eight species of dotillid crabs from Indonesia, and compare them in relation to habitat preferences and molecular phylogeny. Ilyoplax delsmani, Ilyoplax orientalis, and Ilyoplax strigicarpus have comparatively simple shapes of their median and lateral teeth, with fewer teeth on each lateral tooth plate compared to Dotilla myctiroides, Dotilla wichmanni, Scopimera gordonae, Scopimera intermedia, and Tmethypocoelis aff. ceratophora, which have more complexly shaped median and lateral teeth, with a greater number of teeth on each lateral tooth plate. The number of teeth on lateral tooth correlates with habitat preference, that is, dotillid crabs inhabiting muddy substrata have fewer teeth on the lateral tooth plate, and those inhabiting sandy substrata have a more teeth. Phylogenetic analysis using partial COI and 16S rRNA genes supports that teeth morphology is similar among closely related species. Therefore, the description of median and lateral teeth of the gastric mill is expected to contribute to the systematic study of dotillid crabs.

Specific tumour-associated methylation in normal human term placenta and first-trimester cytotrophoblasts.

Human placentation displays many similarities with tumourigenesis, including rapid cell division, migration and invasion, overlapping gene expression profiles and escape from immune detection. Recent data have identified promoter methylation in the Ras association factor and adenomatous polyposis coli tumour suppressor genes as part of this process. However, the extent of tumour-associated methylation in the placenta remains unclear. Using whole genome methylation data as a starting point, we have examined this phenomenon in placental tissue. We found no evidence for methylation of the majority of common tumour suppressor genes in term placentas, but identified methylation in several genes previously described in some human tumours. Notably, promoter methylation of four independent negative regulators of Wnt signalling has now been identified in human placental tissue and purified trophoblasts. Methylation is present in baboon, but not in mouse placentas. This supports a role for elevated Wnt signalling in primate trophoblast invasiveness and placentation. Examination of invasive choriocarcinoma cell lines revealed altered methylation patterns consistent with a role of methylation change in gestational trophoblastic disease. This distinct pattern of tumour-associated methylation implicates a coordinated series of epigenetic silencing events, similar to those associated with some tumours, in the distinct features of normal human placental invasion and function.

Methylation of the adenomatous polyposis coli (APC) gene in human placenta and hypermethylation in choriocarcinoma cells.

Methylation of the human APC gene promoter is associated with several different types of cancers and has also been documented in some pre-cancerous tissues. We have examined the methylation of APC gene promoters in human placenta and choriocarcinoma cells. This revealed a general hypomethylation of the APC-1b promoter and a pattern with monoallelic methylation of the APC-1a promoter in full term placental tissue. However, there was no evidence of a parent-of-origin effect, suggesting random post zygotic origin of methylation. Increased methylation of this promoter was observed in all choriocarcinoma-derived trophoblast cell lines, suggesting a trophoblastic origin of placental APC methylation and implicating APC hypermethylation in the development of this group of gestational tumours. Our demonstration of placental methylation of the APC-1a promoter represents the first observation of monoallelic methylation of this gene in early development, and provides further support for a role of canonical Wnt signalling in placental trophoblast invasiveness. This also implicates tumour suppressor gene silencing as an integral part of normal human placental development.