An improved and expanded nomenclature for genetic sequences is introduced that corresponds with a ranking of the reliability of the taxonomic identification of the source specimens. This nomenclature is an advancement of the “Genetypes” naming system, which some have been reluctant to adopt because of the use of the “type” suffix in the terminology. In the new nomenclature, genetic sequences are labeled “genseq,” followed by a reliability ranking (e.g., 1 if the sequence is from a primary type), followed by the name of the genes from which the sequences were derived (e.g., genseq-1 16S, COI). The numbered suffix provides an indication of the likely reliability of taxonomic identification of the voucher. Included in this ranking system, in descending order of taxonomic reliability, are the following: sequences from primary types – “genseq-1,” secondary types – “genseq-2,” collection-vouchered topotypes – “genseq-3,” collection-vouchered non-types – “genseq-4,” and non-types that lack specimen vouchers but have photo vouchers – “genseq-5.” To demonstrate use of the new nomenclature, we review recently published new-species descriptions in the ichthyological literature that include DNA data and apply the GenSeq nomenclature to sequences referenced in those publications. We encourage authors to adopt the GenSeq nomenclature (note capital “G” and “S” when referring to the nomenclatural program) to provide a searchable tag (e.g., “genseq”; note lowercase “g” and “s” when referring to sequences) for genetic sequences from types and other vouchered specimens. Use of the new nomenclature and ranking system will improve integration of molecular phylogenetics and biological taxonomy and enhance the ability of researchers to assess the reliability of sequence data. We further encourage authors to update sequence information on databases such as GenBank whenever nomenclatural changes are made.

Alveolar rhabdomyosarcoma (ARMS) patients have a poor prognosis, and this is primarily due to overexpression of the oncogenic fusion protein PAX3-FOXO1. Results of RNA-sequencing studies show that PAX3-FOXO1 represses expression of interleukin-24 (IL24), and these two genes are inversely expressed in patient tumors. PAX3-FOXO1 also regulates histone deacetylase 5 (HDAC5) in ARMS cells, and results of RNA interference studies confirmed that PAX3-FOXO1-mediated repression of IL24 is HDAC5-dependent. Knockdown of PAX3-FOXO1 decreases ARMS cell proliferation, survival, and migration, and we also observed similar responses in cells after overexpression of IL24, consistent with results reported for this tumor suppressor-like cytokine in other solid tumors. We also observed in double knockdown studies that the inhibition of ARMS cell proliferation, survival, and migration after knockdown of PAX3-FOXO1 was significantly (>75%) reversed by knockdown of IL24. Adenoviral-expressed IL24 was directly injected into ARMS tumors in athymic nude mice, and this resulted in decreased tumor growth and weight. Because adenoviral IL24 has already successfully undergone phase I in clinical trials, this represents an alternative approach (alone and/or combination) for treating ARMS patients who currently undergo cytotoxic drug therapies.

The length–weight relationships (LWR) of the common seadragon Phyllopteryx taeniolatus (Lacepède, 1804) and the leafy seadragon Phycodurus eques (Günther, 1865), Syngnathidae, are presented in this paper, based on specimens raised in the Birch Aquarium at Scripps, La Jolla, California. Furthermore, we used the length at known age of 40 specimens of common and 15 leafy seadragons to estimate the parameter of the von Bertalanffy growth function (VBGF) for these species. Some of the pros and cons of the newly proposed length type used, ‘scalene length’ are presented. The parameters of the LWR and the VBGF parameters are discussed, with an emphasis on the rearing conditions, the peculiar anatomy of seadragons, especially of P. eques, and on the Gill-Oxygen Limitation Theory (GOLT).

<p>Antibodies, oligonucleotides and primers</p>

<p>Immunostaining of Rh30 and Rh18 cells after transfection with pCMV-6-IL-24</p>