Using bioinformatics and experimental validation, we obtained a cDNA (named srsf) which was exclusively expressed in the mouse testes. RT-PCR analysis showed that srsf mRNA was not expressed in the gonad during the sex determination period or during embryogenesis. In developing mouse tests, srsf expression was first detected on post-natal day 10, reached its highest level on day 23, and then reduced to and remained at a moderate level throughout adulthood. In situ hybridization analysis demonstrated that srsf mRNA was expressed in pachytene spermatocytes and round spermatids in the testes. The predicted protein contains one RNA-binding domain (RBD) and a serine-arginine rich domain (RS), which are characterized by some splicing factors of SR family members. These findings indicate that srsf may play a role during spermatogenesis.
Two tapeworm specimens collected in northeast China in 2009 and 2011 were identified as Diphyllobothrium latum based on morphological criteria. Molecular methods were used to confirm their identity and analyze genetic variations compared with published data for this species. Species identity was confirmed by molecular characterization of the 18S rDNA partial sequence, complete sequences of internal transcribed spacers (ITSs) and 5.8S rDNA, and partial sequences of mitochondrial cytochrome c oxidase subunit 1 (cox1) and mitochondrial NADH dehydrogenase subunit 5 (nad5). PCR amplification and sequence analysis of 18S rDNA (1472 bp), ITS regions (1218 bp), cox1 (885 bp), and nad5 (1028 bp) revealed that these four sequences showed more than 99% identity to reference sequences for D. latum, confirming that this species is D. latum. To date, a total of 12 diphyllobothriosis cases have been documented in China. This study represents the first molecular characterization of D. latum in China, providing molecular evidence of human diphyllobothriosis in China.
Soluble APRIL (sAPRIL), the active form of a proliferation-inducing ligand (APRIL), is implicated in the proliferation of tumor cells. Suppressing APRIL function has been considered as a potential strategy for the therapy of APRIL-associated tumors. In the present study, we generated human sAPRIL and its two mutants, Gln187-D-sAPRIL (Gln187 deleted) and Gly187-sAPRIL (Gln187 replaced by Gly). In vitro experiments showed that the two mutants had similar specific binding capacity to lung carcinoma A549 cells compared to the wild-type sAPRIL, and both, especially Gly187-sAPRIL, exhibited significant antagonistic effect on sAPRIL-induced tumor cell proliferation in a dose-dependent manner, which might be predominantly mediated by blocking sAPRIL-induced MEK and ERK phosphorylation but not p38MAPK or JNK signaling. In vivo experiments with nude mice bearing A549 cell-derived xenograft tumor showed that only the Gly187-sAPRIL mutant could significantly suppress the tumor growth. These results suggest that Gln187 may be a crucial amino acid in APRIL-mediated tumor cell proliferation via the MEK-ERK signaling pathway and that the sAPRIL mutants may serve as novel potential antagonists of APRIL for the therapy of APRIL-associated cancers.