A new species of the dentipes-subgroup of Triconia and a redescription of T. giesbrechti and T. elongata (Copepoda: Cyclopoida: Oncaeidae) from the tropical Pacific and the Korea Strait

A new species of Triconia in the family Oncaeidae, Triconia pacifica sp. nov., and a new form variant each of Triconia giesbrechti Böttger-Schnack and Triconia elongata Böttger-Schnack are described from two sites in the Pacific. Triconia pacifica can be distinguished from its sibling Triconia dentipes (Giesbrecht) by (1) morphometric characters, including the proportional lengths of distal endopod spines of swimming leg 4, and the relative length of the outer basal seta on P5, and by (2) a number of micro-structures on the appendages. The Pacific specimens of T. elongata and T. giesbrechti resemble the typical forms in morphometric characters, with some minor differences in proportional spine lengths on the swimming legs, and differ in a few micro-structures. The hitherto unknown male of T. giesbrechti is newly described. For all species/forms described, the intraspecific variability of proportional spine lengths on the endopods of P2–P4 is examined and discussed. http://www.zoobank.org/urn:lsid:zoobank.org:pub:6B41B0E2-0A5C-458B-8F9C-25000F208E24     

Suppressor of cytokine signaling 1 blocks mitosis in human melanoma cells

Hypermethylation of SOCS genes is associated with many human cancers, suggesting a role as tumor suppressors. As adaptor molecules for ubiquitin ligases, SOCS proteins modulate turnover of numerous target proteins. Few SOCS targets identified so far have a direct role in cell cycle progression; the mechanism by which SOCS regulate the cell cycle thus remains largely unknown. Here we show that SOCS1 overexpression inhibits in vitro and in vivo expansion of human melanoma cells, and that SOCS1 associates specifically with Cdh1, triggering its degradation by the proteasome. Cells therefore show a G1/S transition defect, as well as a secondary blockade in mitosis and accumulation of cells in metaphase. SOCS1 expression correlated with a reduction in cyclin D/E levels and an increase in the tumor suppressor p19, as well as the CDK inhibitor p53, explaining the G1/S transition defect. As a result of Cdh1 degradation, SOCS1-expressing cells accumulated cyclin B1 and securin, as well as apparently inactive Cdc20, in mitosis. Levels of the late mitotic Cdh1 substrate Aurora A did not change. These observations comprise a hitherto unreported mechanism of SOCS1 tumor suppression, suggesting this molecule as a candidate for the design of new therapeutic strategies for human melanoma.