Vivipary in the cactus family: A reply to Ortega-Baes` et al. evaluation of 25 species from northwestern Argentina

This is a reply to Ortega-Baes` et al. (2010) survey of 25 Argentinean species of cacti evaluated for vivipary. We argue that the sample size and geographic area of the species investigated is insufficient to totally exclude the putative commonness of this condition in the Cactaceae. We indicate possible reasons why they did not find viviparous fruits in their survey. Failure to detect vivipary in cacti of NW Argentina may be correlated with limited taxonomic sampling and geographic region in addition to intrinsic and extrinsic plant factors, including different stages of fruit and seed development and genetic, ecological, and edaphic aspects, which, individually or in concert, control precocious germination. We uphold that viviparity is putatively frequent in this family and list 16 new cases for a total of 53 viviparous cacti, which make up ca. 4% incidence of viviparism in the Cactaceae, a substantially higher percentage than most angiosperm families exhibiting this condition. The Cactaceae ranks fourth in frequency of viviparity after the aquatic families of mangroves and seagrasses. We suggest the re-evaluation of cactus vivipary, primarily as a reproductive adaptation to changing environments and physiological stress with a secondary role as a reproductive strategy with limited offspring dispersal/survival and fitness advantages. (C) 2011 Elsevier Ltd. All rights reserved.

Peptide gomesin triggers cell death through L-type channel calcium influx, MAPK/ERK, PKC and PI3K signaling and generation of reactive oxygen species

Gomesin is an antimicrobial peptide isolated from hemocytes of a common Brazilian tarantula spider named Acanthoscurriagomesiana. This peptide exerts antitumor activity in vitro and in vivo by an unknown mechanism. In this study, the cytotoxic mechanism of gomesin in human neuroblastoma SH-SY5Y and rat pheochromocytoma PC12 cells was investigated. Gomesin induced necrotic cell death and was cytotoxic to SH-SY5Y and PC12 cells. The peptide evoked a rapid and transient elevation of intracellular calcium levels in Fluo-4-AM loaded PC12 cells, which was inhibited by nimodipine, an L-type calcium channel blocker. Preincubation with nimodipine also inhibited cell death induced by gomesin in SH-SY5Y and PC12 cells. Gomesin-induced cell death was prevented by the pretreatment with MAPK/ERK, PKC or PI3K inhibitors, but not with PKA inhibitor. In addition, gomesin generated reactive oxygen species (ROS) in SH-SY5Y cells, which were blocked with nimodipine and MAPK/ERK, PKC or PI3K inhibitors. Taken together, these results suggest that gomesin could be a useful anticancer agent, which mechanism of cytotoxicity implicates calcium entry through L-type calcium channels, activation of MAPK/ERK, PKC and PI3K signaling as well as the generation of reactive oxygen species. (C) 2010 Elsevier Ireland Ltd. All rights reserved.