Could the elongate yellow-orange nostrils of Anguilla bicolor McClelland, 1844 function as fishing lures?

The shortfin eel Anguilla bicolor has elongate, yellow nostrils tipped with orange that protrude forward above the mouth. They are a striking, highly visible feature and it is hypothesised that they function as lures to attract prey, analogous to the illicium and esca of anglerfishes and frogfishes and the lingual appendage of the alligator snapping turtle. Another possible function is as an intraspecific signalling device. The first hypothesis is favoured here.     

Genomic investigation of phenotypic variation in Campylobacter jejuni flagellin.

Western blots of whole-cell sonicates of 10 different clones of a faecal isolate of Campylobacter jejuni 533 detected the expression of flagella antigens of either 59 or 62 kDa. Other antigenic proteins appeared identical both in the parent and all the clones. The mechanism for this phenotypic variation was studied using Southern blotting with a flagellin-specific gene probe and products of a polymerase chain reaction (PCR) using flagellin-gene primers. Restriction-enzyme digestion and Southern blotting did not detect any genomic rearrangements in the flagellin genes of the different phenotypes nor did restriction-enzyme analysis of the PCR products.     

Animal models in the study of vomiting

The emetic responses to various pharmacological agents, cytotoxins, and radiation are compared among animal species. The species included for comparison are the human, nonhuman primate, dog, cat, and ferret. The categories of pharmacologic compounds include both those compounds that act on identified membrane receptors (e.g., cholinergic agonists, catecholamines, and neuroactive peptides) and those that act on unidentified receptors (e.g., cardiac glycosides and Veratrum alkaloids, among others). Emphasis is placed on emetic dose-response relations and threshold ED50 and ED100 values calculated from these relations, as indices of species sensitivity to emetic stimuli. For the more noxious emetics, the cytotoxins and radiation, the latency to the first emetic episode and duration of emesis are also compared across species. The effect that peripheral and central nerve lesions have on species differences in emetic responses to stimuli is also discussed.     

Chromosomal Localization, Embryonic Expression, and Imprinting Tests for Bmp7 on Distal Mouse Chromosome 2

Murine Bmp7 has been assigned to distal Chromosome 2 by interspecific backcross mapping. The map location suggests close linkage to classical mouse mutations and places Bmp7 within a chromosome region thought to contain one or more unidentified imprinted genes. A direct test suggests that Bmp7 is not imprinted. An examination of embryonic RNA expression patterns shows that Bmp7 is expressed in a variety of skeletal and nonskeletal tissues. Both embryonic expression patterns and the human chromosomal sublocalization inferred from its mouse location make Bmp7 a candidate for the gene affected in some patients with Holt-Oram syndrome.     

Pleiotropic action of the murine quaking locus: Structure of the qk v allele

The spontaneous allele quaking^viable (qk ^v ) exerts effects on myelination and spermiogenesis. The defects generated by qk ^v were not separated in a multilocus mapping cross that provided a mapping resolution of 0.1 centiMorgans (cM). Furthermore, no distortions suggestive of a large chromosomal anomaly associated with qk ^v were apparent. One plausible interpretation is that the quaking locus contains more than one functional domain, either organized into overlapping genes or expressed by alternative splicing mechanisms. The cloning needed to analyze this locus will be enhanced by the very high resolution of the meiotic mapping cross reported here. The recombinational distances on this qk ^v map were compressed compared with those previously reported in a high-resolution map for qk ^1–1, an embryonic lethal allele of quaking induced by ethylnitrosourea. Additional crosses confirmed prior reports that the sex and the genetic background of the heterozygous parent can affect recombinational distances. These joint effects on recombination are strong enough to account for the discrepancy between the two maps. This variability of two-factor map values leads to the preferred multilocus map-building protocol discussed in the accompanying paper.     

Interaction between Hsc70 and DnaJ homologues: relationship between Hsc70 polymerization and ATPase activity.

We previously found that, in the presence of ATP, DnaJ homologues catalytically induce formation of a metastable Hsc70 polymer and, similarly, the DnaJ homologue auxilin catalytically induces formation of a metastable Hsc70-clathrin basket complex. Since this suggests that the induction of metastable complexes, which form in ATP but dissociate in ADP, may be a general property of DnaJ homologues, in the present study we investigated in more detail the ability of DnaJ homologues to induce polymerization of Hsc70. This study shows that DnaJ homologues induce polymerization of Hsc70 at the same rate as they induce an initial burst of Hsc70 ATPase activity, showing that polymerization is a specific effect of DnaJ homologue binding to Hsc70. However, polymerization does not always accompany the initial burst of ATPase activity. The dependence of the rates of ATPase activity and polymerization on DnaJ homologue concentration shows that DnaJ homologues bind very weakly to Hsc70 in the presence of ATP and do not bind at all in ADP. Surprisingly, however, under certain conditions the rate of polymerization appears to be independent of Hsc70 concentration, suggesting that polymerization is a first-order reaction, perhaps occurring when two Hsc70 molecules bind to a single DnaJ molecule and then shift their binding to each other. We propose that both the polymerization of Hsc70 by DnaJ homologues and the presentation of substrate by DnaJ homologues to Hsc70 involve the bringing of substrate into proximity with Hsc70 and then independently inducing rapid ATP hydrolysis to cause formation of a metastable Hsc70-substrate complex.     

Genome-wide programmable transcriptional memory by CRISPR-based epigenome editing

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Obesity-inducing lesions of the central nervous system alter leptin uptake by the blood-brain barrier.

Leptin regulates body adiposity by decreasing feeding and increasing thermogenesis. Obese humans and some obese rodents are resistant to peripherally administered leptin, suggesting a defect in the transport of leptin across the blood-brain barrier (BBB). Defective transport of exogenous leptin occurs in some models of obesity, but in other models transport is normal. This shows that factors other than obesity are associated with impairment of leptin transport across the BBB. In order to further investigate these factors, we determined leptin transport in rats made obese by lesioning of the ventromedial hypothalamus (VMH), paraventricular nucleus (PVN), or posterodorsal amygdala (PDA). These regions all contain leptin receptors and lesions there induce obesity and hyperleptinemia and alter the levels of many feeding hormones which might participate in leptin transporter regulation. We measured the uptake of radioactively labeled leptin by the BBB by multiple-time regression analysis which divides uptake into a reversible phase (Vi, e.g., receptor/transporter binding to the brain endothelial cell) and an irreversible phase (Ki, complete transport across the BBB). Leptin uptake was not affected in rats with VMH lesions. No significant change occurred in the entry rate (Ki) for any group, although Ki declined by over 35% in rats with PVN lesions. Decreased uptake was observed in rats with PVN lesions and with PDA lesions. This was primarily due to a reduced Vi (about 21% for the PDA). This decreased uptake is most likely explained by decreased binding of leptin to the brain endothelial cell, which could be because of decreased binding by either receptors or transporters. This suggests that some of the feeding hormones controlled by the PVN and PDA may participate in regulating leptin uptake by the BBB.