Salinity Preference in the Estuarine Teleost Fish Mummichog (Fundulus heteroclitus): Halocline Behavior.

Mummichogs prefer seawater (SW) but have wide ability to acclimate to extreme temperatures and salinities. In the field, minnow trapping revealed that mummichogs move progressively into low-salinity warmer water during early spring after ice melt and show significant aversion to colder temperatures and high salinity. First appearance in estuarine shallows occurred above 10°C, and catch increased to 21°C over 4 wk. Three-spine sticklebacks (Gasterosteus aculeatus) also preferred warmer low-salinity locations but preferred slowing streams, whereas mummichogs preferred tidal ponds. In the laboratory, artificial haloclines tested isothermal salinity preference, between 28‰ full-strength SW (below) and 10% SW (3.0‰; above). Mummichogs of both sexes acclimated to 5°C in SW strongly preferred SW. Freshwater (0% SW)-acclimated mummichogs at 21°C also preferred SW, but of sexually mature fish acclimated to 21°C SW, only the males preferred SW; the females showed no significant preference for SW, meaning they freely entered low salinity. SW preference was manifested by a stereotypic passive aversion to the dilute upper layer at the halocline. We conclude that the overall movement of mummichogs into summer breeding grounds of low salinity is driven by maturation of females and their preference for warmer water regardless of salinity.

Mutations in the retinoblastoma-related gene RB2/p130 in primary nasopharyngeal carcinoma.

Nasopharyngeal carcinoma (NPC) is an endemic cancer in southern China and northern Africa, and its pathogenesis is not yet well defined at the molecular level. Although the involvement of p53 and of the retinoblastoma gene (RB/p105) in NPC has been well studied, there is paucity of mutational data regarding the retinoblastoma-related gene RB2/p130 in primary tumors and particularly in NPC. We have shown previously that RB2/p130 could be rearranged in a nasopharyngeal cell line. In the present study, we screened by single-strand conformation polymorphism and sequence analysis the retinoblastoma-related gene RB2/p130 for mutations within exons 19-22. Mutations in the RB2/p130 gene were detected in 3 of 10 primary human NPCs from Northern Africa (30%). These findings, along with previous data showing that genetic replacement of RB2/p130 restores a normal growth pathway in the nasopharyngeal cell line Hone-1, strengthen the hypothesis that genetic changes of RB2/p130 may be involved in the development and/or progression of nasopharyngeal cancer and suggest that RB2/p130 could be considered a tumor suppressor gene and may be a candidate for novel gene therapeutic approaches for NPC.

Ectopic expression of decorin protein core causes a generalized growth suppression in neoplastic cells of various histogenetic origin and requires endogenous p21, an inhibitor of cyclin-dependent kinases.

Decorin belongs to a family of secreted, small, leucine-rich proteoglycans that affect matrix assembly and cellular growth. Ectopic expression of decorin proteoglycan or protein core as a mutated form lacking any glycosaminoglycan side chains induced growth suppression in neoplastic cells of various histogenetic origins, including tumor cells derived from gastrointestinal, genital, skeletal, cutaneous, or bone marrow tissues. Exogenously added recombinant decorin also suppressed overall growth of the parental cell lines. In all stably-transfected clones, growth retardation was specifically associated with induction of the potent cyclin-dependent kinase inhibitor p21, but not p27, and subsequent translocation of p21 protein into the nuclei of decorin-expressing cells. This led to a greater proportion of the cells arrested in G1 phase of the cell cycle. These changes were independent of functional p53 or retinoblastoma protein. De novo expression of decorin in HCT116 human colon carcinoma cells harboring a disrupted p21 gene failed to induce growth suppression, in contrast to the wild-type cells in which p21 and growth arrest could be induced. These findings indicate that ectopic production of decorin protein core can retard the growth of a variety of tumor cells and that endogenous p21 is a required downstream effector of this biological axis.