ABSTRACT
The brown alga Sargassum provides a natural substrate occupied by hydrozoans in shallow marine waters. A global count in 2007 listed 39 epibiotic species of Hydrozoa growing on Sargassum, but more studies have been published since, therefore, an update is timely, particularly due to the increased abundance of Sargassum in the Caribbean. This review, based on a recent literature survey and new records from Mexico, includes 133 publications of epibiotic hydrozoans on Sargassum spanning 220 years, from 1802 to 2022. A total of 131 hydrozoan species were recorded on 26 species of Sargassum, most belonging to the subclass Hydroidolina (130), with only one record of a trachyline medusa (Gonionemus vertens, subclass Trachylinae). Most publications centered on the Tropical Atlantic, where the greatest number of hydrozoan species (67 species) were recorded. All hydrozoan species possess a hydrorhiza, except one hydromedusae species that attach to Sargassum via adhesive tentacles. Most of the hydrozoan species associated with Sargassum exhibited a benthic life cycle (93 species) and are comprised of erect, branched colonies (67 species) and large hydrothecae (69 species). Although the number of studies of epibiotic hydrozoans on Sargassum has increased since the mid-20th century, nevertheless hydrozoan richness has not reached an asymptote. Therefore, more sampling of Sargassum species would likely identify more hydrozoan species associated with Sargassum, especially among benthic Sargassum, and might help reveal potential biogeographical and ecological patterns between Sargassum and hydrozoan epibionts.
Subject(s)
Hydrozoa , Sargassum , Animals , Life Cycle Stages , Caribbean Region , MexicoABSTRACT
Previous results showed that GnRH signaling is altered in cells from rat luteinized ovarian tumors (tumor group) because it did not activate the phospholipase C pathway, in contrast to control ovarian cells from superovulated prepubertal rats (SPO). In the present work, alternate GnRH-induced second messengers such as phospholipase A(2) and phospholipase D activation, cAMP production, ERK1/2 phosphorylation, and the presence of G proteins were evaluated to determine GnRH mechanism of action in tumor cells. G proteins examined were present in both cell types. Buserelin, a GnRH agonist, (1, 10, and 100 ng/ml) increased phosphatidylethanol in SPO, indicating phospholipase D activation. Only 100 ng/ml buserelin induced a significant response in the tumor group. Buserelin (100 ng/ml) increased (3)H-arachidonic acid in culture media in SPO, indicating phospholipase A(2) activation; no effect was observed in the tumor group. Buserelin (100 and 1000 ng/ml) induced pertussis toxin-insensitive cAMP increases in both cell types, with similar potencies. In the tumor group, buserelin (100 ng/ml) inhibited human chorionic gonadotropin-induced cAMP and progesterone; this effect was protein kinase C (PKC) dependent (inhibited by GF109203X, a PKC inhibitor). Buserelin (100 and 1000 ng/ml) induced ERK1/2 phosphorylation in both cell kinds. Buserelin-induced ERK1/2 activation was G(i/0) independent and PKC dependent. Only in the tumor group, buserelin-induced ERK1/2 activation was cAMP dependent (abolished by SQ 22536, the adenylyl cyclase inhibitor). Furthermore, dibutyryl cAMP-induced ERK1/2 activation in the tumor group was PKC dependent (inhibited by GF109203X). In conclusion, activation of phospholipases in tumor cells does not seem to mediate GnRH effects. GnRH signaling seems to involve adenylyl cyclase activation, PKC stimulation, and ERK1/2 phosphorylation.