Human sperm do not bind to rat zonae pellucidae despite the presence of four homologous glycoproteins

The specificity of sperm-egg recognition in mammals is mediated primarily by the zona pellucida surrounding ovulated eggs. Mouse sperm are quite promiscuous and bind to human eggs, but human spermatozoa will not bind to mouse eggs. The mouse zona pellucida contains three glycoproteins, ZP1, ZP2, and ZP3, which are conserved in rat and human. The recent observation that human zonae pellucidae contain a fourth protein raises the possibility that the presence of four zona proteins will support human sperm binding. Using mass spectrometry, four proteins that are similar in size and share 62-70% amino acid identity with human ZP1, ZP2, ZP3, and ZP4/ZPB were detected in rat zonae pellucidae. However, although mouse and rat spermatozoa bind to eggs from each rodent, human sperm bind to neither, and the presence of human follicular fluid did not alter the specificity of sperm binding. In addition, mutant mouse eggs lacking hybrid/complex N-glycans or deficient in Core 2 O-glycans were no more able to support human sperm binding than normal mouse eggs. These data suggest that the presence of four zona proteins are not sufficient to support human sperm binding to rodent eggs and that additional determinants must be responsible for taxon-specific fertilization among mammals.     

Membrane traffic in animal cells: cellular glycoproteins return to the site of Golgi mannosidase I

The recycling of cellular glycoproteins to the site of Golgi mannosidase I, an enzyme of asparagine-linked oligosaccharide synthesis, was studied in K562 human erythroleukemia cells. Cells were metabolically labeled in the presence of deoxymannojirimycin, a reversible inhibitor of Golgi mannosidase I. This generates glycoproteins with immature oligosaccharides in their normal locations. Transport to the mannosidase I compartment was then assessed by testing for the conversion of oligosaccharides into mature forms during reculture without deoxymannojirimycin. Transferrin receptor (TfR) was acted on by mannosidase I during reculture, suggesting that it returned to the region of the Golgi complex where this enzyme resides. The slow rate of this transport (t1/2 greater than 6 h) implies that it is probably different than TfR movement during transferrin internalization (t1/2 = 10-20 min) and TfR transport to the sialyltransferase compartment in the Golgi complex (t1/2 = 2-3 h) (Snider, M. D., and O. C. Rogers, 1985, J. Cell Biol., 100:826-834). The total cell glycoprotein pool was also transported to the mannosidase I compartment with a half-time of 4 h. Because this transport is 5-10 times faster than the rate of de novo glycoprotein synthesis in these cells, it is likely that most of the glycoprotein traffic through the Golgi complex is composed of recycling molecules.     

A comprehensive review of epinephrine in the finger: to do or not to do.

The prohibition against the use of local anesthetics with epinephrine for digital blocks or infiltration is an established surgical tradition. The present article provides a comprehensive review of all reported digital necrotic and ischemic complications with epinephrine in the digits in an effort to understand whether the current prohibition is based on documented reports. A comprehensive review of articles showing the successful use of local anesthetic with epinephrine in the digits is presented.A review of Index Medicus from 1880 to 1966 and a computer review of the National Library of Medicine database from 1966 to 2000 were performed using multiple keywords. Selected major textbooks from 1900 to 2000 were also reviewed.A total of 48 cases of digital gangrene after anesthetic blocks (mostly using cocaine or procaine) have been reported in the world literature. Only 21 cases involved the use of epinephrine; 17 involved an unknown concentration based on manual dilution. Multiple other concurrent conditions (hot soaks, tight tourniquets, and infection) existed in these case reports, making it difficult to determine the exact cause of the tissue insult. There have been no case reports of digital gangrene using commercial lidocaine with epinephrine (introduced in 1948). Multiple studies involving thousands of patients support the premise that the use of lidocaine with epinephrine is safe in the digits.An extensive literature review failed to provide consistent evidence that our current preparations of local anesthesia with epinephrine cause digital necrosis, although not all complications are necessarily reported. However, as with all techniques, caution is necessary to balance the risks of this technique with the dangers of mechanical tourniquets and upper extremity block anesthesia.     

Beta-COP localizes mainly to the cis-Golgi side in exocrine pancreas

We examined the distribution of the non-clathrin-coated vesicle- associated coat protein beta-COP in rat exocrine pancreatic cells by immunogold cytochemistry. Labeling for beta-COP was found in the Golgi region (48%) where it was associated with vesicles and buds of approximately 50 nm, showing a characteristic approximately 10-nm-thick coat. The other half of the label was present in the cytoplasm, not associated with visible coats or membranes, with a minor fraction present on small clusters of tubules and vesicles. Clathrin-coated vesicles were typically located at the trans-side of the Golgi complex, and showed a thicker coat of approximately 18 nm. Of the total beta-COP labeling over the Golgi region, 68% occurred on the cis-side, 6% on the cisternae, 17% on the rims of the cisternae, and only 9% on the trans- side. For clathrin these figures were 16, 2, 4, and 78%, respectively. At the cis-Golgi side beta-COP was present in transitional areas (TA), on so-called peripheral elements (PE), consisting of tubules and vesicles located between the cup-shaped transitional elements (TE) of the RER and the cis-most Golgi cisternae. Label for Sec23p was also present in TA but was located closer to the TE, while beta-COP labeled PE were located near the cis-Golgi cisternae. Upon energy depletion, Golgi associated beta-COP was almost exclusively (86%) in spherical aggregates of 200-500 nm in diameter, whereas the cis-side (6%), the cisternae (1%), the rims (4%) and trans-side (3%) of the Golgi complex, were barely labeled; 50% of the total label remained in the cytoplasm. The aggregates were predominantly located at the cis-side of the Golgi stack, next to, but distinct from the Sec23p positive TA, that were devoid of beta-COP and had only a few recognizable vesicles left. Incubation with aluminum fluoride resulted in fragmentation of the Golgi complex into large clusters of beta-COP positive vesicles, while 50% of the label remained in the cytoplasm, as in control cells. After 10 min of Brefeldin A treatment 91% of beta-COP was cytoplasmic and only 7% associated with membranes of the Golgi complex. The total label for beta-COP over exocrine cells remained unchanged during the incubation with either of the drugs, indicating that the drugs induce reallocation of beta-COP. Our data suggest that beta-COP plays a role in membrane transport at the cis-side of the Golgi complex.     

Sleeping birds do not respond to predator odour

Background

During sleep animals are relatively unresponsive and unaware of their environment, and therefore, more exposed to predation risk than alert and awake animals. This vulnerability might influence when, where and how animals sleep depending on the risk of predation perceived before going to sleep. Less clear is whether animals remain sensitive to predation cues when already asleep.

Methodology/Principal Findings

We experimentally tested whether great tits are able to detect the chemical cues of a common nocturnal predator while sleeping. We predicted that birds exposed to the scent of a mammalian predator (mustelid) twice during the night would not go into torpor (which reduces their vigilance) and hence would not reduce their body temperature as much as control birds, exposed to the scent of another mammal that does not represent a danger for the birds (rabbit). As a consequence of the higher body temperature birds exposed to the scent of a predator are predicted to have a higher resting metabolic rate (RMR) and to lose more body mass. In the experiment, all birds decreased their body temperature during the night, but we did not find any influence of the treatment on body temperature, RMR, or body mass.

Conclusions/Significance

Our results suggest that birds are not able to detect predator chemical cues while sleeping. As a consequence, antipredatory strategies taken before sleep, such as roosting sites inspection, may be crucial to cope with the vulnerability to predation risk while sleeping.     

Racial discrimination: How not to do it

The UNESCO Statements on Race of the early 1950s are understood to have marked a consensus amongst natural scientists and social scientists that ‘race’ is a social construct. Human biological diversity was shown to be predominantly clinal, or gradual, not discreet, and clustered, as racial naturalism implied. From the seventies social constructionists added that the vast majority of human genetic diversity resides within any given racialised group. While social constructionism about race became the majority consensus view on the topic, social constructionism has always had its critics. Sesardic (2010) has compiled these criticisms into one of the strongest defences of racial naturalism in recent times. In this paper I argue that Sesardic equivocates between two versions of racial naturalism: a weak version and a strong version. As I shall argue, the strong version is not supported by the relevant science. The weak version, on the other hand, does not contrast properly with what social constructionists think about ‘race’. By leaning on this weak view Sesardic’s racial naturalism intermittently gains an appearance of plausibility, but this view is too weak to revive racial naturalism. As Sesardic demonstrates, there are new arguments for racial naturalism post-Human Genome Diversity Project. The positive message behind my critique is how to be a social constructionist about race in the post-genomic era.     

Maturation of lipoprotein lipase. Expression of full catalytic activity requires glucose trimming but not translocation to the cis-Golgi compartment.

The relationship between maturation of lipoprotein lipase (LPL) and its translocation from the endoplasmic reticulum (ER) to the Golgi complex was determined by measuring lipolytic activity under conditions preventing transport of the enzyme from the ER to the Golgi compartment. In the presence of brefeldin A, a reagent that inhibits movement of proteins from the ER and causes the disassembly of the Golgi complex, pro-5 Chinese hamster ovary cells accumulated catalytically active LPL, while secretion of the enzyme was effectively blocked. LPL retained intracellularly by brefeldin A treatment possessed oligosaccharide chains that were processed to the complex form by the Golgi enzymes redistributed into the ER. At 16 degrees C, a condition disrupting protein transport to the cis-Golgi, the retained enzyme again remained catalytically active although the oligosaccharides remained in the high mannose form. Lastly, attachment of the specific ER retention signal KDEL (Lys-Asp-Glu-Leu) to the carboxyl terminus of LPL also resulted in intracellularly retained enzyme that was fully active. The importance of oligosaccharide processing for attainment of LPL catalytic activity in vitro was also determined. LPL was active and secreted when trimming of the mannose residues was inhibited by deoxymannojirimycin and when addition of complex sugars was blocked using Chinese hamster ovary mutants (lec1 and lec2), indicating that these processing events are not necessary for the expression of a functional enzyme. However, blocking glucose removal by glucosidase inhibitors (castanospermine and N-methyl-deoxynojirimycin) resulted in a significant reduction in LPL specific activity and secretion. Thus, glucose trimming of LPL oligosaccharides is essential for enzyme activation; however, further oligosaccharide processing or translocation of the enzyme to the cis-Golgi is not required for full expression of lipolytic activity in vitro.     

Chimpanzees know what conspecifics do and do not see

We report a series of experiments on social problem solving in chimpanzees, Pan troglodytes. In each experiment a subordinate and a dominant individual were put into competition over two pieces of food. In all experiments dominants obtained virtually all of the foods to which they had good visual and physical access. However, subordinates were successful quite often in three situations in which they had better visual access to the food than the dominant, for example, when the food was positioned so that only the subordinate (and not the dominant) could see it. In some cases, the subordinate might have been monitoring the behaviour of the dominant directly and simply avoided the food that the dominant was moving towards (which just happened to be the one it could see). In other cases, however, we ruled out this possibility by giving subordinates a small headstart and forcing them to make their choice (to go to the food that both competitors could see, or the food that only they could see) before the dominant was released into the area. Together with other recent studies, the present investigation suggests that chimpanzees know what conspecifics can and cannot see, and, furthermore, that they use this knowledge to devise effective social-cognitive strategies in naturally occurring food competition situations. Copyright 2000 The Association for the Study of Animal Behaviour.