Echinoids (sea urchins) are divided into two major groups -cidaroids (a 'primitive' group) and euechinoids (a 'derived' group). The cidaroids are a promising model species for understanding the ancestral developmental mechanisms in echinoids, but little is known about the molecular mechanisms of cidaroid development. In euechinoids, skeletogenic mesenchyme cell specification is regulated by the double-negative gate (DNG), in which hesC represses the transcription of the downstream mesenchyme specification genes (alx1, tbr and ets1), thereby defining the prospective mesenchyme region. To estimate the ancestral mechanism of larval mesenchyme cell specification in echinoids, the expression patterns and roles of mesenchyme specification genes in the cidaroid Prionocidaris baculosa were examined. The present study reveals that the expression pattern and function of hesC in P. baculosa were inconsistent with the DNG model, suggesting that the euechinoidtype DNG is not utilized during cidaroid mesenchyme specification. In contrast with hesC, the expression patterns and functions of alx1, tbr and ets1 were similar between P. baculosa and euechinoids. Based on these results, we propose that the roles of alx1, tbr and ets1 in mesenchyme specification were established in the common ancestor of echinoids, and that the DNG system was acquired in the euechinoid lineage after divergence from the cidaroid ancestor. The evolutionary timing of the establishment of the DNG suggests that the DNG was originally related to micromere and/or primary mesenchyme cell formation but not to skeletogenic cell differentiation.

Dried apple peels were extracted with n-hexane, chloroform, and methanol successively. The portion of the chloroform extract that showed the strongest cytotoxic activity was purified by silica gel chromatography to isolate ursolic acid (UA). The amount of the isolated UA was 0.71% of the dried peels. Normal mouse embryo cells [serum-free mouse embryo (SFME) cells] and tumorigenic human c-Haras-and mouse c-myc-transformed SFME cells [r/m highly metastatic (HM)-SFME-1 cells] were treated with various concentrations of UA (2.5-20 µM) to investigate its effects on cell growth. UA at 10 µM appeared very effective at suppressing the tumor cell growth, affecting more than 82% of r/m HM-SFME-1 cells, while it inhibited cell growth in only about 7% of SFME cells. Tumorigenic r/m HM-SFME-1 cells were also treated with various concentrations (2.5-10 µM) of epidermal growth factor (EGF) or aminoguanidine (AG) in the presence of UA (2.5-10 µM). Neither EGF nor AG seemed to have any effect on UA-inhibited cell growth. In the present study, it is revealed that UA could be a very effective and promising agent for antitumor treatments, * To whom correspondence should be addressed: Department of Pharmacy, Faculty of Pharmacy, Meijo University, 150 Yagotoyama, Tenpaku, Nagoya 468-8503, Japan. Tel.: +81-52-839-2721; Fax: +81-52-834-8090; E-mail: hyamagu@ccmfs. meijo-u.ac.jp as it specifically affects tumorigenic cells yet appears to cause very little harm to normal cells.

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