Cuticular compounds inhibit cannibalism of early-instar spiderlings by pulli-carrying Pardosa pseudoannulata females.

Cannibalism is common in spiders. Wolf spider (Lycosidae) females, which exhibit extensive maternal care, have been reported to cannibalize less when they are carrying egg sacs and juveniles. In a laboratory experiment, we demonstrated that cannibalism of early-instar spiderlings (EIS) by a wolf spider (Pardosa pseudoannulata) mother was almost completely inhibited when she was carrying spiderlings. Compared with virgin and mated-females, mother spiders tolerated more and predated fewer spiderlings, including gregarious pulli and newly dispersed spiderlings (NDS). Cannibalism of EIS by females during their reproductive period exhibited a V-shaped pattern, with a gradual decrease from the egg sac-carrying to pulli-carrying (PC) stage, and a recovery from the PC stage to post-reproductive (PR) stage. Notably, there was 0 cannibalism at the PC stage. PC females exhibited no interest in pulli, while PR females were attracted to and predated pulli and NDS as they did their natural prey, Nilaparvata lugens. Interestingly, PC females captured and released NDS in a foraging assay, although attraction was observed from olfactometer measurements. PC mothers possessed a cuticular volatile profile that was closer to that of pulli and NDS than to that of PR females. Moreover, NDS cuticular extract provoked an electrophysiological response in legs of PC females. Therefore, cuticular compound-mediated chemical communication may be involved in inhibiting cannibalism of EIS by spider mothers, and especially in eliminating cannibalism by PC mothers. Future studies will aim to characterize the specific cuticular compounds and chemoreception mechanism in females, which will facilitate our understanding of intraspecific recognition and cannibalism in spiders.

PmtA functions as a ferrous iron and cobalt efflux pump in Streptococcus suis.

Transition metals are nutrients essential for life. However, an excess of metals can be toxic to cells, and host-imposed metal toxicity is an important mechanism for controlling bacterial infection. Accordingly, bacteria have evolved metal efflux systems to maintain metal homeostasis. Here, we established that PmtA functions as a ferrous iron [Fe(II)] and cobalt [Co(II)] efflux pump in Streptococcus suis, an emerging zoonotic pathogen responsible for severe infections in both humans and pigs. pmtA expression is induced by Fe(II), Co(II), and nickel [Ni(II)], whereas PmtA protects S. suis against Fe(II) and ferric iron [Fe(III)]-induced bactericidal effect, as well as Co(II) and zinc [Zn(II)]-induced bacteriostatic effect. In the presence of elevated concentrations of Fe(II) and Co(II), ΔpmtA accumulates high levels of intracellular iron and cobalt, respectively. ΔpmtA is also more sensitive to streptonigrin, a Fe(II)-activated antibiotic. Furthermore, growth defects of ΔpmtA under Fe(II) or Co(II) excess conditions can be alleviated by manganese [Mn(II)] supplementation. Finally, PmtA plays a role in tolerance to H2O2-induced oxidative stress, yet is not involved in the virulence of S. suis in mice. Together, these data demonstrate that S. suis PmtA acts as a Fe(II) and Co(II) efflux pump, and contributes to oxidative stress resistance.

CopA Protects Streptococcus suis against Copper Toxicity.

Streptococcus suis is a zoonotic pathogen that causes great economic losses to the swine industry and severe threats to public health. A better understanding of its physiology would contribute to the control of its infections. Although copper is an essential micronutrient for life, it is toxic to cells when present in excessive amounts. Herein, we provide evidence that CopA is required for S. suis resistance to copper toxicity. Quantitative PCR analysis showed that copA expression was specifically induced by copper. Growth curve analyses and spot dilution assays showed that the ΔcopA mutant was defective in media supplemented with elevated concentrations of copper. Spot dilution assays also revealed that CopA protected S. suis against the copper-induced bactericidal effect. Using inductively coupled plasma-optical emission spectroscopy, we demonstrated that the role of CopA in copper resistance was mediated by copper efflux. Collectively, our data indicated that CopA protects S. suis against the copper-induced bactericidal effect via copper efflux.

miRNA-34c inhibits myoblasts proliferation by targeting YY1.

miRNAs are increasingly being implicated as key regulators of cell proliferation, apoptosis, and differentiation. miRNA-34c appears to play a crucial role in cancer pathogenesis wherein it exerts its effect as a tumor suppressor. However, the role of miR-34c in myoblast proliferation remains poorly understood. Here, we found that overexpression miR-34c inhibited myoblasts proliferation by reducing the protein and mRNA expression of cell cycle genes. In contrast, blocking the function of miR-34c promoted myoblasts proliferation and increased the protein and mRNA expression of cell cycle genes. Moreover, miR-34c directly targeted YY1 and inhibited its expression. Similar to overexpression miR-34c, knockdown of YY1 by siRNA suppressed myoblasts proliferation. Our study provides novel evidence for a role of miR-34c in inhibiting myoblasts proliferation by repressing YY1. Thus, miR-34c has the potential to be used to enhance skeletal muscle development and regeneration.