Cdc2-like kinase 2 (Clk2) promotes early neural development in Xenopus embryos.

Neural induction and patterning in vertebrates are regulated during early development by several morphogens, such as bone morphogenetic proteins (BMPs) and fibroblast growth factors (FGFs). Ventral ectoderm differentiates into epidermis in response to BMPs, whereas BMP signaling is tightly inhibited in the dorsal ectoderm which develops into neural tissues. Here, we show that Cdc2-like kinase 2 (Clk2) promotes early neural development and inhibits epidermis differentiation in Xenopus embryos. clk2 is specifically expressed in neural tissues along the anterior-posterior axis during early Xenopus embryogenesis. When overexpressed in ectodermal explants, Clk2 induces the expression of both anterior and posterior neural marker genes. In agreement with this observation, overexpression of Clk2 in whole embryos expands the neural plate at the expense of epidermal ectoderm. Interestingly, the neural-inducing activity of Clk2 is increased following BMP inhibition and activation of the FGF signaling pathway in ectodermal explants. Clk2 also downregulates the level of p-Smad1/5/8 in cooperation with BMP inhibition, in addition to increasing the level of activated MAPK together with FGF. These results suggest that Clk2 plays a role in early neural development of Xenopus possibly via modulation of morphogen signals such as the BMP and FGF pathways.

Involvement of JunB Proto-Oncogene in Tail Formation During Early Xenopus Embryogenesis.

Integration of signaling pathways is important for the establishment of the body plan during embryogenesis. However, little is known about how the multiple signals interact to regulate morphogenesis. Here, we show that junb is expressed in the posterior neural plate and the caudal fin during Xenopus embryogenesis and that overexpression of wild-type JunB induces small head phenotypes and ectopic tail-like structures. A mutant form of JunB that lacked GSK3 and MAPK phosphorylation sites showed stronger tail-like structure-inducing activity than wild-type JunB. Moreover, the mutant JunB induced expression of tailbud and neural marker genes, but not somite and chordoneural hinge (CNH) marker genes in ectopic tail-like structures. In ectodermal explants of Xenopus embryos, overexpression of JunB increased the expression of tailbud and posterior marker genes including fgf3, xbra (t) and wnt8. These results indicate that JunB is capable of inducing the ectopic formation of tissues similar to the tailbud, and that the tailbud-inducing activity of JunB is likely to be regulated by FGF and Wnt pathways. Overall, our results suggest that JunB is a regulator of tail organization possibly through integration of several morphogen signaling pathways.

Erratum to: Rats demonstrate helping behavior toward a soaked conspecific.

Erratum to: Anim CognDOI 10.1007/s10071-015-0872-2. The authors would like to correct the word "less" to "more" in the sentence under the heading "Results and discussion". The correct sentence should read as: This indicates that the soaked rats spent more time in the pool area than did the helper rats.

Rats demonstrate helping behavior toward a soaked conspecific.

Helping behavior is a prosocial behavior whereby an individual helps another irrespective of disadvantages to him or herself. In the present study, we examined whether rats would help distressed, conspecific rats that had been soaked with water. In Experiment 1, rats quickly learned to liberate a soaked cagemate from the water area by opening the door to allow the trapped rat into a safe area. Additional tests showed that the presentation of a distressed cagemate was necessary to induce rapid door-opening behavior. In addition, it was shown that rats dislike soaking and that rats that had previously experienced a soaking were quicker to learn how to help a cagemate than those that had never been soaked. In Experiment 2, the results indicated that rats did not open the door to a cagemate that was not distressed. In Experiment 3, we tested behavior when rats were forced to choose between opening the door to help a distressed cagemate and opening a different door to obtain a food reward. Irrespective of how they learned to open the door, in most test trials, rats chose to help the cagemate before obtaining a food reward, suggesting that the relative value of helping others is greater than the value of a food reward. These results suggest that rats can behave prosocially and that helper rats may be motivated by empathy-like feelings toward their distressed cagemate.

Oxytocin administration modulates rats' helping behavior depending on social context.

The affiliative effect of oxytocin on behavior toward other individuals can be modulated by positive and negative aspects of those individuals. However, the context-dependent effect of oxytocin on helping behavior is still unclear. In this study, we examined the effect of oxytocin administration on helping behavior in rats. The rats learned to open a door to help a cagemate soaked with water. The rats were divided into Pair and Solo groups. The rats in the Pair group were housed with their cagemates and those in the Solo group were housed individually. The rats in both groups received oxytocin (1.0 mg/kg) or saline injections intraperitoneally for 5 consecutive days before starting the experimental sessions. In the rats injected with oxytocin, the Solo group showed helping behavior faster than those in the Pair group. The results suggest that the effects of oxytocin administration on helping behavior are dependent on the social context.

Sex differences in circadian food anticipatory activity are not altered by individual manipulations of sex hormones or sex chromosome copy number in mice.

Recent studies in mice have demonstrated a sexual dimorphism in circadian entrainment to scheduled feeding. On a time restricted diet, males tend to develop food anticipatory activity (FAA) sooner than females and with a higher amplitude of activity. The underlying cause of this sex difference remains unknown. One study suggests that sex hormones, both androgens and estrogens, modulate food anticipatory activity in mice. Here we present results suggesting that the sex difference in FAA is unrelated to gonadal sex hormones. While a sex difference between males and females in FAA on a timed, calorie restricted diet was observed there were no differences between intact and gonadectomized mice in the onset or magnitude of FAA. To test other sources of the sex difference in circadian entrainment to scheduled feeding, we used sex chromosome copy number mutants, but there was no difference in FAA when comparing XX, XY-, XY-;Sry Tg, and XX;Sry Tg mice, demonstrating that gene dosage of sex chromosomes does not mediate the sex difference in FAA. Next, we masculinized female mice by treating them with 17-beta estradiol during the neonatal period; yet again, we saw no difference in FAA between control and masculinized females. Finally, we observed that there was no longer a sex difference in FAA for older mice, suggesting that the sex difference in FAA is age-dependent. Thus, our study demonstrates that singular manipulations of gonadal hormones, sex chromosomes, or developmental patterning are not able to explain the difference in FAA between young male and female mice.