Inbreeding and experience affect response to climate change by endangered woodpeckers

In recent decades, female red-cockaded woodpeckers (Picoides borealis) have laid eggs increasingly earlier in response to a changing climate, as has been observed in several other bird species breeding at north temperate latitudes. Within each year, females that lay earlier are more productive than females that lay later. However, inexperienced females, experienced females who change mates and inbred birds have not adjusted to the changing climate by laying earlier, and have suffered reproductive costs as a result. Failure to respond to global climate change may be a further example of the reduced ability of inbred animals to respond to environmental challenges.     

What kind of signals do mimetic tiger moths send? A phylogenetic test of wasp mimicry systems (Lepidoptera: Arctiidae: Euchromiini).

Mimicry has been examined in field and laboratory studies of butterflies and its evolutionary dynamics have been explored in computer simulations. Phylogenetic studies examining the evolution of mimicry, however, are rare. Here, the phylogeny of wasp-mimicking tiger moths, the Sphecosoma group, was used to test evolutionary predictions of computer simulations of conventional Müllerian mimicry and quasi-Batesian mimicry dynamics. We examined whether mimetic traits evolved individually, or as suites of characters, using concentrated change tests. The phylogeny of these moth mimics revealed that individual mimetic characters were conserved, as are the three mimetic wasp forms: yellow Polybia, black Polybia and Parachartergus mimetic types. This finding was consistent with a 'supergene' control of linked loci and the Nicholson two-step model of mimicry evolution. We also used a modified permutation-tail probability approach to examine the rate of mimetic-type evolution. The observed topology, hypothetical Müllerian and Batesian scenarios, and 1000 random trees were compared using Kishino-Hasegawa tests. The observed phylogeny was more consistent with the predicted Müllerian distribution of mimetic traits than with that of a quasi-Batesian scenario. We suggest that the range of discriminatory abilities of the predator community plays a key role in shaping mimicry dynamics.     

Evidence for infanticide in bottlenose dolphins of the western North Atlantic

Nine bottlenose dolphin (Tursiops truncatus) calves that stranded in Virginia in 1996 and 1997 died of severe blunt-force trauma. Injuries were concentrated on the head and chest and multiple rib fractures, lung lacerations, and soft tissue contusions were prominent. Skeletal and/or soft tissue trauma occurred bilaterally in all of the calves. One had a bite wound across the left mandible that exhibited deep punctures consistent with the tooth placement in an adult bottlenose dolphin. The lesions were not compatible with predation, boat strike, fisheries interactions, rough-surf injury, or blast injury. However, they were similar to traumatic injuries described in stranded bottlenose dolphin calves and harbor porpoises (Phocoena phocoena) in Great Britain attributed to violent dolphin interactions. The evidence suggests that violent dolphin behavior was the cause of the trauma in the nine calves reported here and that infanticide occurs in bottlenose dolphins of the western North Atlantic.     

Differences in reactivity of antibodies to active versus inactive PLTP significantly impacts PLTP measurement

Due to conflicting reports concerning the relationship between phospholipid transfer protein (PLTP) activity and mass in plasma, the protein concentration and activity of PLTP were assessed in fractions isolated by fast protein liquid chromatography from the plasma of healthy normolipidemic individuals. Using both polyclonal and monoclonal antibodies, PLTP was identified by Western blot analysis after both SDS and non-denaturing gradient gel electrophoresis, and quantitated by dot blot. PLTP activity was determined using a labeled vesicle/HDL assay. PLTP mass corresponded substantially with the activity distribution using the polyclonal antibody on dot blot with some inactive PLTP being present. However, the monoclonal antibody preferentially reacted with inactive PLTP, primarily associated with LDL and large HDL, overestimating inactive PLTP. Western blot analysis of non-denaturing gradient gels, using the polyclonal antibody, indicated that active PLTP was associated with numerous discrete HDL subpopulations (7.6-12.0 nm) with the major portion being 9-12 nm. Inactive PLTP was associated with particles of 12 to >17 nm. The monoclonal antibody demonstrated a different pattern of reactivity on gradient gels, showing strong reactivity with the inactive PLTP in particles of 12 to >17 nm, but less reactivity with particles of 7.6-12 nm. The differences in reactivities of antibodies for active versus inactive PLTP can account for some of the discrepancies reported in the literature regarding the relationship between PLTP mass and activity.     

Comparison of the folding processes of T. thermophilus and E. coli ribonucleases H

In order to examine how the stabilization of thermophilic proteins affects their folding, we have characterized the folding process of Thermus thermophilus ribonuclease H using circular dichroism, fluorescence, and pulse-labeling hydrogen exchange. Like its homolog from Escherichia coli, this thermophilic protein populates a partially folded kinetic intermediate within the first few milliseconds of folding. The structure of this intermediate is similar to that of E.coli RNase H and corresponds remarkably well to a partially folded form that is populated at low levels in the native state of the protein. Proline isomerization appears to partly limit the folding of the thermophilic but not the mesophilic protein. Lastly, unlike other thermophilic proteins, which unfold much more slowly than their mesophilic counterparts, T.thermophilus RNase H folds and unfolds with overall rates similar to those of E.coli RNase H.     

Overexpression of the signaling adapter FRS2 reconstitutes the cell cycle deficit of a nerve growth factor non-responsive TrkA receptor mutant

We have characterized the cell cycle deficit of a novel TrkA receptor mutant (TrkAS3) that fails to support nerve growth factor (NGF)-dependent cell cycle arrest and neurite outgrowth. TrkAS3 receptors fail to support an NGF-dependent increase in the expression of cyclin D1 and the cell cycle inhibitor, p21(Waf1/Cip1), two important regulators of G(1) /S transition, and do not down-regulate expression of the G(2) /M phase marker, cdc2/cdk1, or the S phase marker, proliferating cell nuclear antigen. Moreover, NGF-activated TrkAS3 receptors do not down-regulate cyclin-dependent kinase 4 phosphorylation of the retinoblastoma protein, essential for G(1) arrest, in comparison to NGF-activated wild-type TrkA. Collectively these data indicate that TrkAS3 receptors fail to support NGF-dependent G(1) arrest. Interestingly, ectopic expression of regulators of G(1) /S arrest, such as cyclin D1 or inhibitors of cell cycle (p21(Waf1/Cip1), p16(INK4A) ), or the fibroblast growth factor (FGF) receptor substrate-2 (FRS2) in cells expressing TrkAS3 reconstitutes NGF-dependent neurite outgrowth. Collectively, these data suggest a model in which NGF-stimulated TrkA-dependent activation of FRS2 supports neurite outgrowth through a mechanism that likely involves the induction of p21(Waf1/Cip1) expression and the arrest of cells at G(1) /S.     

Mutant membrane protein of the budding yeast spindle pole body is targeted to the endoplasmic reticulum degradation pathway

Mutation of either the yeast MPS2 or the NDC1 gene leads to identical spindle pole body (SPB) duplication defects: The newly formed SPB is improperly inserted into the nuclear envelope (NE), preventing the cell from forming a bipolar mitotic spindle. We have previously shown that both MPS2 and NDC1 encode integral membrane proteins localized at the SPB. Here we show that CUE1, previously known to have a role in coupling ubiquitin conjugation to ER degradation, is an unusual dosage suppressor of mutations in MPS2 and NDC1. Cue1p has been shown to recruit the soluble ubiquitin-conjugating enzyme, Ubc7p, to the cytoplasmic face of the ER membrane where it can ubiquitinate its substrates and target them for degradation by the proteasome. Both mps2-1 and ndc1-1 are also suppressed by disruption of UBC7 or its partner, UBC6. The Mps2-1p mutant protein level is markedly reduced compared to wild-type Mps2p, and deletion of CUE1 restores the level of Mps2-1p to nearly wild-type levels. Our data indicate that Mps2p may be targeted for degradation by the ER quality control pathway.     

Different phenotypes in vivo are associated with ATPase motif mutations in Schizosaccharomyces pombe minichromosome maintenance proteins

The six conserved MCM proteins are essential for normal DNA replication. They share a central core of homology that contains sequences related to DNA-dependent and AAA(+) ATPases. It has been suggested that the MCMs form a replicative helicase because a hexameric subcomplex formed by MCM4, -6, and -7 proteins has in vitro DNA helicase activity. To test whether ATPase and helicase activities are required for MCM protein function in vivo, we mutated conserved residues in the Walker A and Walker B motifs of MCM4, -6, and -7 and determined that equivalent mutations in these three proteins have different in vivo effects in fission yeast. Some mutations reported to abolish the in vitro helicase activity of the mouse MCM4/6/7 subcomplex do not affect the in vivo function of fission yeast MCM complex. Mutations of consensus CDK sites in Mcm4p and Mcm7p also have no phenotypic consequences. Co-immunoprecipitation analyses and in situ chromatin-binding experiments were used to study the ability of the mutant Mcm4ps to associate with the other MCMs, localize to the nucleus, and bind to chromatin. We conclude that the role of ATP binding and hydrolysis is different for different MCM subunits.