Astropectinid seastars typically develop as either feeding bipinnaria larvae or nonfeeding, barrel‐shaped larvae. Understanding the direction and frequency of evolutionary transitions between these larval nutritional modes requires knowledge of the distribution of developmental diversity in the family, but the development of only a few astropectinids is known. Here we describe embryogenesis, larval development, and metamorphosis of Astropecten armatus, an astropectinid common in soft‐sediment subtidal habitats in southern California. Adults were reproductively mature all year except during the winter months (December–February). Oocytes averaged 137 μm in diameter, the smallest reported in the genus. Fertilized oocytes developed into feeding bipinnaria larvae that fed in the plankton for at least 4 weeks, and in some cases up to 33 weeks, before metamorphosis. The tube feet of juveniles were adhesive, but lacked suckers, contrary to some previous descriptions of suckered tube feet in the juveniles of paxillosidans.
A hallmark of Niemann-Pick disease, type C (NPC) is the progressive degeneration of Purkinje neurons in the cerebellum caused by the accumulation of free cholesterol and glycosphingolipids in the lysosome. Recent studies suggest that the state of glycosylation of lysosomal membrane proteins may play a role in disease progression. Our study has identified the presence of a highly glycosylated form of Lysosome Associated Membrane Protein 1 (LAMP1) that correlated spatiotemporally with Purkinje neuron loss. This form of LAMP1 was predominantly localized to activated microglia; showing a~5-fold increase in surface labeling by FACS analysis. This suggests a potential role for LAMP1 in the neuro-inflammatory process in these mice during disease progression. Analysis of other mouse models of neurodegeneration that exhibit neuro-inflammation showed little or no presence of this glycosylated form of LAMP1, suggesting this observation for LAMP1 is specific to NPC disease. Furthermore, early treatment of Npc1 -/mice with 2-hydroxypropyl-β-cyclodextrin (HPβCD), significantly prevented the appearance of the glycosylated LAMP1 in the cerebellum of Npc1 -/mice at 7 weeks, consistent with the prevention of neuro-inflammation in mice treated with this drug. Treatment of Npc1 -/mice with HPβCD at 7 weeks, after disease onset, did not reverse or prevent further appearance of the hyperglycosylated LAMP1, demonstrating that once this aspect of neuro-inflammation began, it continued despite the HPβCD treatment. Analysis of LAMP1 in cerebellar tissue of NPC1 patients showed a small level of hyperglycosylated LAMP1 in the tissue, however, this was not seen in the CSF of patients.
Macrophage dysfunction in the BALB/c Npc1 mouse is similar to that observed in other Crohn disease models. However, neither the degree of pathology nor the microbiota changes are typical of Crohn disease. Thus, this mouse model is not a good model system for Crohn disease pathology reported in NPC1 patients.
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