Influence of body size on fecundity and sperm management in the parasitoid wasp Anisopteromalus calandrae

A large body size is considered to be advantageous to the reproductive success of females as a result of several factors, such as the allocation of more resources to reproduction and the efficient management of sperm transferred by males. In the present study, the effects of female body size, female mating status and additional food availability on fecundity and the offspring sex ratio are investigated in the parasitoid wasp Anisopteromalus calandrae Howard (Hymenoptera: Pteromalidae). Because of haplodiploid sex determination, females must fertilize eggs to produce female offspring but not to produce male offspring. As predicted, female fecundity and the number of female offspring are positively correlated with body size. However, although the volume of the spermatheca increases with female body size, the amount of sperm stored in the spermatheca is relatively constant, irrespective of body size. Consequently, larger females produce a greater proportion of male offspring, especially at the end of the oviposition sequence, suggesting that larger females that possess more resources for reproduction and produce a larger number of offspring are more likely to suffer sperm depletion. The results of the present study also show that mated females have an increased fecundity compared with virgin females, although the opportunity to feed on honey along with host feeding has no impact upon fecundity or the sex ratio.     

Localization of swine PRE-1 homologues in 13 loci of Phacochoerus aethiopicus and Tayassu tajacu genomes, and their sequence divergence

In our previous study, PRE-1 (a swine short interspersed nuclear element, SINE) was found to be present in the genomes of animal species related to swine ( Sus scrofa ) i.e. warthog ( Phacochoerus aethiopicus ) and collared peccary ( Tayassu tajacu ) at almost the same frequency as in Sus scrofa . In the present study, we investigated whether PRE-1 was present in hippopotamus ( Hippopotamus amphibius ), which is in the same order but in a different family to Sus scrofa . Hippopotamus amphibius was found to contain no PRE-1. Then, in order to study the localization of PRE-1 sequences at locus level and the sequence divergence of the PRE-1 of individual loci among Sus scrofa , Phacochoerus aethiopicus and Tayassu tajacu , primer sets, which can amplify PRE-1 sequences at 13 loci of swine genome with the polymerase chain reaction, were prepared to identify any corresponding sequences in Phacochoerus aethiopicus and Tayassu tajacu . Twelve and nine of the 13 primer sets identified fragments in Phacochoerus aethiopicus and Tayassu tajacu respectively. Ten of the 12 Phacochoerus aethiopicus fragments and two of the nine Tayassu tajacu fragments contained PRE-1 sequences. Based on the divergence between the corresponding PRE-1 sequences at individual loci and on the mutation rate of the pseudogenes (r=4·6×10^–9), Phacochoerus aethiopicus and Tayassu tajacu are currently calculated to have been separated from Sus scrofa later than 1·4million years before present (MYBP) and 16·8 MYBP, respectively.     

Lysophosphatidylcholine Acyltransferase1 Overexpression Promotes Oral Squamous Cell Carcinoma Progression via Enhanced Biosynthesis of Platelet-Activating Factor

Background

The relevance of lysophosphatidylcholine acyltransferase1 (LPCAT1), a cytosolic enzyme in the remodeling pathway of phosphatidylcholine metabolism, in oral squamous cell carcinoma (OSCC) is unknown. We investigated LPCAT1 expression and its functional mechanism in OSCCs.

Methods

We analyzed LPCAT1 mRNA and protein expression levels in OSCC-derived cell lines. Immunohistochemistry was performed to identify correlations between LPCAT1 expression levels and primary OSCCs clinicopathological status. We established LPCAT1 knockdown models of the OSCC-derived cell lines (SAS, Ca9-22) for functional analysis and examined the association between LPCAT1 expression and the platelet-activating factor (PAF) concentration and PAF-receptor (PAFR) expression.

Results

LPCAT1 mRNA and protein were up-regulated significantly (p<0.05) in OSCC-derived cell lines compared with human normal oral keratinocytes. Immunohistochemistry showed significantly (p<0.05) elevated LPCAT1 expression in primary OSCCs compared with normal counterparts and a strong correlation between LPCAT1-positive OSCCs and tumoral size and regional lymph node metastasis. In LPCAT1 knockdown cells, cellular proliferation and invasiveness decreased significantly (p<0.05); cellular migration was inhibited compared with control cells. Down-regulation of LPCAT1 resulted in a decreased intercellular PAF concentration and PAFR expression.

Conclusion

LPCAT1 was overexpressed in OSCCs and correlated with cellular invasiveness and migration. LPCAT1 may contribute to tumoral growth and metastasis in oral cancer.     

BCG Skin Infection Triggers IL-1R-MyD88-Dependent Migration of EpCAMlow CD11bhigh Skin Dendritic cells to Draining Lymph Node During CD4+ T-Cell Priming

The transport of antigen from the periphery to the draining lymph node (DLN) is critical for T-cell priming but remains poorly studied during infection with Mycobacterium bovis Bacille Calmette-Guérin (BCG). To address this we employed a mouse model to track the traffic of Dendritic cells (DCs) and mycobacteria from the BCG inoculation site in the skin to the DLN. Detection of BCG in the DLN was concomitant with the priming of antigen-specific CD4⁺ T cells at that site. We found EpCAM^low CD11b^high migratory skin DCs to be mobilized during the transport of BCG to the DLN. Migratory skin DCs distributed to the T-cell area of the LN, co-localized with BCG and were found in close apposition to antigen-specific CD4⁺ T cells. Consequently, blockade of skin DC traffic into DLN dramatically reduced mycobacterial entry into DLN and muted T-cell priming. Interestingly, DC and mycobacterial entry into the DLN was dependent on IL-1R-I, MyD88, TNFR-I and IL-12p40. In addition, we found using DC adoptive transfers that the requirement for MyD88 in BCG-triggered migration was not restricted to the migrating DC itself and that hematopoietic expression of MyD88 was needed in part for full-fledged migration. Our observations thus identify a population of DCs that contribute towards the priming of CD4⁺ T cells to BCG infection by transporting bacilli into the DLN in an IL-1R-MyD88-dependent manner and reveal both DC-intrinsic and -extrinsic requirements for MyD88 in DC migration.     

In Vivo Regulation of Erythropoiesis by Chemically Inducible Dimerization of the Erythropoietin Receptor Intracellular Domain

Erythropoietin (Epo) and its receptor (EpoR) are required for the regulation of erythropoiesis. Epo binds to the EpoR homodimer on the surface of erythroid progenitors and erythroblasts, and positions the intracellular domains of the homodimer to be in close proximity with each other. This conformational change is sufficient for the initiation of Epo-EpoR signal transduction. Here, we established a system of chemically regulated erythropoiesis in transgenic mice expressing a modified EpoR intracellular domain (amino acids 247–406) in which dimerization is induced using a specific compound (chemical inducer of dimerization, CID). Erythropoiesis is reversibly induced by oral administration of the CID to the transgenic mice. Because transgene expression is limited to hematopoietic cells by the Gata1 gene regulatory region, the effect of the CID is limited to erythropoiesis without adverse effects. Additionally, we show that the 160 amino acid sequence is the minimal essential domain of EpoR for intracellular signaling of chemically inducible erythropoiesis in vivo. We propose that the CID-dependent dimerization system combined with the EpoR intracellular domain and the Gata1 gene regulatory region generates a novel peroral strategy for the treatment of anemia.