Technical comment on Boersma et al. (2016) Temperature driven changes in the diet preference of omnivorous copepods: no more meat when it's hot? Ecology Letters, 19, 45–53

A recent study concluded that omnivorous plankton will shift from predatory to herbivorous feeding with climate warming, as consumers require increased carbon:phosphorous in their food. Although this is an appealing hypothesis, we suggest the conclusion is unfounded, based on the data presented, which seem in places questionable and poorly interpreted.     

Recycling cell surface glycoproteins undergo limited oligosaccharide reprocessing in LEC1 mutant Chinese hamster ovary cells

The ability of particular cell surface glycoproteins to recycle and become exposed to individual Golgi enzymes has been demonstrated. This study was designed to determine whether endocytic trafficking includes significant reentry into the overall oligosaccharide processing pathway. The Lec1 mutant of Chinese hamster ovary (CHO) cells lack N - acetylglucosaminyltransferase I (GlcNAc-TI) activity resulting in surface expression of incompletely processed Man5GlcNAc2 N -linked oligosaccharides. An oligosaccharide tracer was created by exoglycosylation of cell surface glycoproteins with purified porcine GlcNAc-TI and UDP-[3H]GlcNAc. Upon reculturing, all cell surface glycoproteins that acquired [3H]GlcNAc were acted upon by intracellular mannosidase II, the next enzyme in the Golgi processing pathway of complex N -linked oligosaccharides (t1/2= 3-4 h). That all radiolabeled cell surface glycoproteins were included in this endocytic pathway indicates a common intracellular compartment into which endocytosed cell surface glycoproteins return. Significantly, no evidence was found for continued oligosaccharide processing consistent with transit through the latter cisternae of the Golgi apparatus. These data indicate that, although recycling plasma membrane glycoproteins can be reexposed to individual Golgi-derived enzymes, significant reentry into the overall contiguous processing pathway is not evident.      

Topological studies on the enzymes catalyzing the biosynthesis of Glc-P- dolichol and the triglucosyl cap of Glc3Man9GlcNAc2-P-P-dolichol in microsomal vesicles from pig brain: use of the processing glucosidases I/II as latency markers

In the current model for Glc3Man9GlcNAc2-P-P-Dol assembly, Man5GlcNAc2- P-P-Dol, Man-P-Dol, and Glc-P-Dol are synthesized on the cytoplasmic face of the ER and diffuse transversely to the lumenal leaflet where the synthesis of the lipid-bound precursor oligosaccharide is completed. To establish the topological sites of Glc-P-Dol synthesis and the lipid-mediated glucosyltransfer reactions involved in Glc3Man9GlcNAc2-P-P-Dol synthesis in ER vesicles from pig brain, the trypsin-sensitivity of Glc-P-Dol synthase activity and the Glc-P- Dol:Glc0-2Man9GlcNAc2-P-P-Dol glucosyltransferases (GlcTases) was examined in sealed microsomal vesicles. Since ER vesicles from brain do not contain glucose 6-phosphate (Glc 6-P) phosphatase activity, the latency of the lumenally oriented, processing glucosidase I/II activities was used to assess the intactness of the vesicle preparations. Comparative enzymatic studies with sealed ER vesicles from brain and kidney, a tissue that contains Glc 6-P phosphatase, demonstrate the reliability of using the processing glucosidase activities as latency markers for topological studies with microsomal vesicles from non-gluconeogenic tissues lacking Glc 6-P phosphatase. The results obtained from the trypsin-sensitivity assays with sealed microsomal vesicles from brain are consistent with a topological model in which Glc-P-Dol is synthesized on the cytoplasmic face of the ER, and subsequently utilized by the three Glc-P-Dol-mediated GlcTases after "flip-flopping" to the lumenal monolayer.      

Cuticular reactivity of the early larval stages of Ascaris suum: adhesion and degranulation of polymorphonuclear leukocytes of the surface of opsonized larvae of A. suum.

Binding of serum proteins (opsonization) on the surface of infective and early parasitic larvae of Ascaris suum is necessary to induce the adherence of polymorphonuclear leukocytes (PMN). When larvae are not pretreated in vitro with serum components, PMN do not adhere either to infective stage larvae or to parasitic larvae recovered from non-immune guinea pigs at 16, 25 or 48 h post oral infection. Adhesion of PMN occurs on all larval stages tested when they are first opsonized in vitro with the 7S fraction of immune serum. Opsonization with macroglobulins of immune serum or with Fab fragments of immune 7S protein does not induce the in vitro adherence of PMN. Adhesion of PMN to the larval surface results in reduction of Nitroblue tetrazolium to formazan precipitate at the larval surface, specifically in areas where cells are adherent, indicating oxidative enzyme action at the cuticle/PMN interface.     

E rosette forming lymphoblasts fail to stimulate allogeneic cells in mixed leukocyte culture (MLC)

Summary Lymphoblasts from patients with acute lymphatic leukemia were examined for the presence of surface markers and for their capacity to stimulate allogeneic donors in MLC. Lymphoblasts from eight patients, which made E rosettes, consistently failed to stimulate allogeneic donors on at least three separate occasions despite the vigorous response of these same allogeneic donors to remission cells from the patients.There were eleven patients who had lymphoblasts with no detectable markers or null lymphoblasts. Three of these also failed to stimulate in MLC. The null lymphoblasts from the remaining eight patients produced vigorous allogeneic responses. Since serologic data is now available suggesting that null lymphoblasts from some ALL patients have serologically detectable T cell antigens [16] while others have antigens found predominantly on B cells [20], it is conceivable that the capacity of these cells to stimulate in MLC may distinguish lymphoblasts within the null category with those which fail to stimulate representing early T cell precursors and those which do stimulate being early B cell precursors.     

A feature selection approach for identification of signature genes from SAGE data

Background  

One goal of gene expression profiling is to identify signature genes that robustly distinguish different types or grades of tumors. Several tumor classifiers based on expression profiling have been proposed using microarray technique. Due to important differences in the probabilistic models of microarray and SAGE technologies, it is important to develop suitable techniques to select specific genes from SAGE measurements.