ABSTRACT Growing evidence suggests that parasite-infected prey is more vulnerable to predation. However, the mechanism underlying this phenomenon is obscure. In small mammals, analgesia induced by environmental stressors is a fundamental component of the defensive repertoire, promoting defensive responses. Thus, the reduced analgesia may impair the defensive ability of prey and increase their predation risk. This study aimed to determine whether coccidia infection increases the vulnerability to predation in root voles, Microtus oeconomus (Pallas, 1776), by decreased analgesia. Herein, a predator stimulus and parasitic infection were simulated in the laboratory via a two-level factorial experiment, then, the vole nociceptive responses to an aversive thermal stimulus were evaluated. Further, a field experiment was performed to determine the overwinter survival of voles with different nociceptive responses via repeated live trapping. The coccidia-infected voles demonstrated reduced predator-induced analgesia following exposure to predator odor. Meanwhile, pain-sensitive voles had lower overwinter survival than pain-inhibited voles in enclosed populations throughout the duration of the experiment. Our findings suggest that coccidia infection attenuates predator-induced analgesia, resulting in an increased vulnerability to predation.

BACKGROUND: Ubiquitin Specific Peptidase 39 (USP39) is a 65 kDa SR-related protein involved in RNA splicing. Previous studies showed that USP39 is related with tumorigenesis of human breast cancer cells. RESULTS: In the present study, we investigated the functions of USP39 in human hepatocellular carcinoma (HCC) cell line SMMC-7721. We knocked down the expression of USP39 through lentivirus mediated RNA interference. The results of qRT-PCR and western blotting assay showed that both the mRNA and protein levels were suppressed efficiently after USP39 specific shRNA was delivered into SMMC-7721 cells. Cell growth was significantly inhibited as determined by MTT assay. Crystal violet staining indicated that colony numbers and sizes were both reduced after knock-down of USP39. Furthermore, suppression of USP39 arrested cell cycle progression at G2/M phase in SMMC-7721cells. In addition, Annexin V showed that downregulation of USP39 significantly increased the population of apoptotic cells. CONCLUSIONS: All our results suggest that USP39 is important for HCC cell proliferation and is a potential target for molecular therapy of HCC.

The mouse testis-enriched Znf230 gene, which encodes a type of RING finger protein, is present primarily in the nuclei of spermatogonia, the acrosome and the tail of spermatozoa. To investigate the role of Znf230 in spermatogenesis, we generated Znf230-deficient mice by disrupting Znf230 exon-5 and exon-6 using homologous recombination. The homozygous Znf230-knockout (KO) mice did not exhibit Znf230 mRNA expression and Znf230 protein production. Znf230 KO mice exhibited no obvious impairment in body growth or fertility. Male Znf230 KO mice had integral reproductive systems and mature sperm that were regular in number and shape. The developmental stages of male germ cells of Znf230 KO mice were also normal. We further examined variations in the transcriptomes of testicular tissue between Znf230 KO and wild-type mice through microarray analysis. The results showed that the mRNA level of one unclassified transcript 4921513I08Rik was increased and that the mRNA levels of three other transcripts, i.e., 4930448A20Rik, 4931431B13Rik and potassium channel tetramerisation domain containing 14(Kctd14), were reduced more than two-fold in Znf230 KO mice compared with wild-type mice. Using our current examination techniques, these findings suggested that Znf230 deficiency in mice may not affect growth, fertility or spermatogenesis.