Schooling and swimming behaviors of Hyla semilineata tadpoles (Anura, Hylidae)

The schooling behavior of Hyla semilineata Spix, 1824 tadpoles is described. Experiments were carried out both in the natural environment and under controlled conditions to quantify the constant movement of these tadpoles. Bullfrog tadpoles (Rana catesbeiana Shaw, 1802), similar in size to the H. semilineata larvae, were used as controls in the experiments. Hyla semilineata tadpoles remained stationary for one sixth of the time that the bullfrog tadpoles did and the number of individuals of H. semilineata moving at any given moment was about seven times greater. The schooling behavior and constant swimming behavior of these tadpoles may enhance the effect of their warning coloration

The effect of social interactions on tadpole activity and growth in the British anuran amphibians (Bufo bufo, B-calamita, and Rana temporaria)

Tadpoles of different species of frogs and toads display different tendencies to aggregate. We investigated some of the costs and benefits of aggregating in three British species by examining their behavioural responses to the presence of conspecifics, and by monitoring the performance of tadpoles under different levels of social interaction with other individuals. The common toad (Bufo bufo), an aggregating species, displayed higher levels of activity than the natterjack toad (B. calamita) and common frog (Rana temporaria), two species that form aggregations less frequently. Moreover, out of the three species, only B. bufo increased activity in the presence of conspecifics. In all three species, increased interaction between individuals resulted in increased variation in size. However, average growth rate was affected only in B. bufo, which grew faster when raised in isolation and not interacting with other individuals. Under certain conditions intraspecific competition therefore seems to tie more important than social facilitation, but may lead to average size at metamorphosis being larger within the population. The consequences of intraspecific competition within aggregations mag therefore be different for individuals and populations

Loss of the inactive myotubularin-related phosphatase Mtmr13 leads to a Charcot–Marie–Tooth 4B2-like peripheral neuropathy in mice

Charcot–Marie–Tooth disease type 4B (CMT4B) is a severe, demyelinating peripheral neuropathy characterized by slowed nerve conduction velocity, axon loss, and distinctive myelin outfolding and infolding. CMT4B is caused by recessive mutations in either myotubularin-related protein 2 (MTMR2; CMT4B1) or MTMR13 (CMT4B2). Myotubularins are phosphoinositide (PI) 3-phosphatases that dephosphorylate phosphatidylinositol 3-phosphate (PtdIns3P) and PtdIns(3,5)P2, two phosphoinositides that regulate endosomal–lysosomal membrane traffic. Interestingly, nearly half of the metazoan myotubularins are predicted to be catalytically inactive. Both active and inactive myotubularins have essential functions in mammals and in Caenorhabditis elegans. MTMR2 and MTMR13 are active and inactive PI 3-phosphatases, respectively, and the two proteins have been shown to directly associate, although the functional significance of this association is not well understood. To establish a mouse model of CMT4B2, we disrupted the Mtmr13 gene. Mtmr13-deficient mice develop a peripheral neuropathy characterized by reduced nerve conduction velocity and myelin outfoldings and infoldings. Dysmyelination is evident in Mtmr13-deficient nerves at 14 days and worsens throughout life. Thus, loss of Mtmr13 in mice leads to a peripheral neuropathy with many of the key features of CMT4B2. Although myelin outfoldings and infoldings occur most frequently at the paranode, our morphological analyses indicate that the ultrastructure of the node of Ranvier and paranode is intact in Mtmr13-deficient nerve fibers. We also found that Mtmr2 levels are decreased by ≈50% in Mtmr13-deficient sciatic nerves, suggesting a mode of Mtmr2 regulation. Mtmr13-deficient mice will be an essential tool for studying how the loss of MTMR13 leads to CMT4B2