Establishment of an albino sand rat (Psammomys obesus colony and comparison with the natural coloured animal

The lifespan and fertility of albino sand rats were found to be severely reduced in comparison with a laboratory colony of brown sand rats. The albinos were also much more susceptible to diabetes, as judged by their glucose tolerance. In fact, untreated albinos had a higher incidence of diabetic response than coloured sand rats fed a diabetogenic diet. The albino sand rats reproduced poorly because of a reduction in male fertility. Circulating testosterone levels and seminal vesicle weights were reduced in the albinos. It is speculated that the reduction in reproductive capacity is related to diabetes.     

Pollen on-twine for food provisioning and oviposition of predatory mites in protected crops

The establishment of predatory mites on protected crops is affected by the availability of shelter and alternative food. We suggest that a pollen covered twine, coined here “pollen on-twine”, may provide these necessities when attached to the plant. We evaluated the effect of twine types and two pollen species on the establishment of Euseius scutalis (Athias-Henriot) and Amblyseius swirskii Athias-Henriot on pre-flowering pepper plants in a growth chamber. For both phytoseiids, rayon jute twine was found more beneficial while corn and oak pollen did not differ in their effect. Though populations of both predators were best promoted when twine and pollen were applied separately, E. scutalis population increased by more than tenfold and A. swirskii doubled when plants were applied with pollen on-twine. We propose that after further refining, pollen on-twine can serve as a feasible solution for predatory mite establishment on protected crops.     

Listeria monocytogenes Multidrug Resistance Transporters and Cyclic Di-AMP,Which Contribute to Type I Interferon Induction,Play a Role in Cell Wall Stress

The intracellular bacterial pathogen Listeria monocytogenes activates a robust type I interferon response upon infection. This response is partially dependent on the multidrug resistance (MDR) transporter MdrM and relies on cyclic-di-AMP (c-di-AMP) secretion, yet the functions of MdrM and cyclic-di-AMP that lead to this response are unknown. Here we report that it is not MdrM alone but a cohort of MDR transporters that together contribute to type I interferon induction during infection. In a search for a physiological function of these transporters, we revealed that they play a role in cell wall stress responses. A mutant with deletion of four transporter genes (ΔmdrMTAC) was found to be sensitive to sublethal concentrations of vancomycin due to an inability to produce and shed peptidoglycan under this stress. Remarkably, c-di-AMP is involved in this phenotype, as overexpression of the c-di-AMP phosphodiesterase (PdeA) resulted in increased susceptibility of the ΔmdrMTAC mutant to vancomycin, whereas overexpression of the c-di-AMP diadenylate cyclase (DacA) reduced susceptibility to this drug. These observations suggest a physiological association between c-di-AMP and the MDR transporters and support the model that MDR transporters mediate c-di-AMP secretion to regulate peptidoglycan synthesis in response to cell wall stress.     

Morphogenesis of the developing mammary gland: Stage-dependent impact of adipocytes

Mammary gland development is critically dependent on the interactions between the stromal and the epithelial compartments within the gland. These events are under the control of a complex interplay of circulating and locally acting hormones and growth factors. To analyze the temporal and quantitative contributions of stromal adipocytes, we took advantage of the FAT-ATTAC mice (apoptosis through triggered activation of caspase-8), a model of inducible and reversible loss of adipocytes. This loss can be achieved through the induced dimerization of a caspase-8 fusion protein. In the context of female mice, we can achieve ablation of mammary adipocytes relatively selectively without affecting other fat pads. Under these conditions, we find that adipocytes are essential for the formation of the extended network of ducts in the mammary gland during puberty. Beyond their role in development, adipocytes are also essential to maintain the normal alveolar structures that develop during adulthood. Loss of adipose tissue initiated 2 weeks after birth triggers fewer duct branching points and fewer terminal end buds (TEBs) and also triggers changes in proliferation and apoptosis in the epithelium associated with the TEBs. The reduced developmental pace that adipocyte-ablated glands undergo is reversible, as the emergence of new local adipocytes, upon cessation of treatment, enables the ductal epithelium to resume growth. Conversely, loss of local adipocytes initiated at 7 weeks of age resulted in excessive lobulation, indicating that adipocytes are critically involved in maintaining proper architecture and functionality of the mammary epithelium. Collectively, using a unique model of inducible and reversible loss of adipocytes, our observations suggest that adipocytes are required for proper development during puberty and for the maintenance of the ductal architecture in the adult mammary gland.     

Downregulation of miR-31, miR-155, and miR-564 in chronic myeloid leukemia cells

Background/Aims

MicroRNAs (miRNAs) are short non-coding regulatory RNAs that control gene expression and play an important role in cancer development and progression. However, little is known about the role of miRNAs in chronic myeloid leukemia (CML). Our objective is to decipher a miRNA expression signature associated with CML and to determine potential target genes and signaling pathways affected by these signature miRNAs.

Results

Using miRNA microarrays and miRNA real-time PCR we characterized the miRNAs expression profile of CML cell lines and patients in reference to non-CML cell lines and healthy blood. Of all miRNAs tested, miR-31, miR-155, and miR-564 were down-regulated in CML cells. Down-regulation of these miRNAs was dependent on BCR-ABL activity. We next analyzed predicted targets and affected pathways of the deregulated miRNAs. As expected, in K562 cells, the expression of several of these targets was inverted to that of the miRNA putatively regulating them. Reassuringly, the analysis identified CML as the main disease associated with these miRNAs. MAPK, ErbB, mammalian target of rapamycin (mTOR) and vascular endothelial growth factor (VEGF) were the main molecular pathways related with these expression patterns. Utilizing Venn diagrams we found appreciable overlap between the CML-related miRNAs and the signaling pathways-related miRNAs.

Conclusions

The miRNAs identified in this study might offer a pivotal role in CML. Nevertheless, while these data point to a central disease, the precise molecular pathway/s targeted by these miRNAs is variable implying a high level of complexity of miRNA target selection and regulation. These deregulated miRNAs highlight new candidate gene targets allowing for a better understanding of the molecular mechanism underlying the development of CML, and propose possible new avenues for therapeutic treatment.