Creating morphological diversity in reptilian temporal skull region: A review of potential developmental mechanisms

Reptilian skull morphology is highly diverse and broadly categorized into three categories based on the number and position of the temporal fenestrations: anapsid, synapsid, and diapsid. According to recent phylogenetic analysis, temporal fenestrations evolved twice independently in amniotes, once in Synapsida and once in Diapsida. Although functional aspects underlying the evolution of tetrapod temporal fenestrations have been well investigated, few studies have investigated the developmental mechanisms responsible for differences in the pattern of temporal skull region. To determine what these mechanisms might be, we first examined how the five temporal bones develop by comparing embryonic cranial osteogenesis between representative extant reptilian species. The pattern of temporal skull region may depend on differences in temporal bone growth rate and growth direction during ontogeny. Next, we compared the histogenesis patterns and the expression of two key osteogenic genes, Runx2 and Msx2, in the temporal region of the representative reptilian embryos. Our comparative analyses suggest that the embryonic histological condition of the domain where temporal fenestrations would form predicts temporal skull morphology in adults and regulatory modifications of Runx2 and Msx2 expression in osteogenic mesenchymal precursor cells are likely involved in generating morphological diversity in the temporal skull region of reptiles.     

The Activin A-Dependent Proliferation of PCC3/A/1 Embryonal Carcinoma Cells in Serum-Free Medium

Examination of the growth requirements of murine embryonal carcinoma cells (EC cells) or embryonic stem cells (ES cells) in serum-free medium revealed that PCC3 EC cells required activin A to grow and/or survive in such medium. In the absence of activin A, PCC3 cells began to disintegrate within 3 days under any serum-free conditions examined. P19 and AT805 EC cells grew even in serum-free medium without activin A but their growth rates were slightly facilitated by its addition. F9 EC cells also grew in the medium without activin A and its addition somewhat inhibited their growth rate. Three independently isolated ES cell lines and feeder-dependent PSA-1 EC cells also grew in serum-free medium without activin A if leukemia inhibitory factor (LIF) was supplemented. The addition of activin A had little effect on their growth rates. These findings suggest that PCC3 EC cells are a sort of nutritional mutant requiring activin A, thus making them useful in stidies on the growth regulatory mechanisms of EC/ES cells and/or the action of activin on EC/ES cells.     

Hybridization experiment betweenGnathopogon elongatus elongatus ♀ andCarassius carassius ♂

Hybrids from an intersubfamilial cross betweenGnathopogon elongatus elongatus ♀ andCarassius carassius ♂ were analyzed morphologically and karyologically and compared with the parental species. These hybrids possessed a mosaic of character expressions that showed overall intermediacy though surperficial appearances were similar toG. elongatus elongatus. Their karyotype was constituted of one genome of theCarassius parent and two genomes of theGnathopogon parent.     

In vitro study of the insulin-like action of vanadyl-pyrone and -pyridinone complexes with a VO(O4) coordination mode

The insulin-like action of a novel class of potential insulin-mimetic complexes was investigated in terms of free fatty acid (FFA) release from isolated rat adipocytes. Vanadyl complexes such as VO(ema)2 [(bis(2-ethyl-3-hydroxy-4-pyrone)VO], VO(mpp)2 [bis (3-hydroxy-2-methyl-4(1H)-pyridinone)VO], VO(dmpp)2 [bis(1,2-dimethyl-3-hydroxy-4(1H)-pyridinone)VO] and VO(empp)2 [bis(2-ethyl-3-hydroxy-1-methyl-4(1H)-pyridinone)VO] were tested together with vanadyl sulfate for comparison. The inhibitory effect of the vanadium complexes on FFA release, from rat adipocytes treated with epinephrine, is dependent on concentration and for that reason the results are reported in terms of the IC50 value, the 50% inhibition concentration. The results show that all the complexes have an inhibitory effect on FFA release and that two pyridinone complexes, VO(mpp)2 and VO(empp)2, have a significantly better insulin-mimetic activity than that of vanadyl sulfate.