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S Ward

Publications and source records attributed to S Ward.

At least 289 records · Page 16Linked to original sources
PubMed1982

Centripetal flow of pseudopodial surface components could propel the amoeboid movement of Caenorhabditis elegans spermatozoa.

Latex beads and wheat germ agglutinin (WGA) were used to examine the movement of membrane components on amoeboid spermatozoa of Caenorhabditis elegans. The behavior of beads attached to the cell revealed continuous, directed movement from the tip of the pseudopod to its base, but no movement on the cell body. Lectin receptors are also cleared from the pseudopod (4). Blocking preexisting lectin receptors with unlabeled WGA followed by pulse-labeling wih fluorescent WGA showed that new lectin receptors are continuously inserted at the tip of the pseudopod. Like latex beads, these new lectin receptors move continuously over the pseudopod surface to the cell body-pseudopod junction where they are probably internalized. Mutants altering the rate of membrane flow, and eliminating its topographical asymmetry, have been identified. Together with the observation that fluorescent phospholipids are cleared from the pseudopod of developing spermatozoa at the same rate as lectin receptors (25), these results show that there is bulk membrane flow over the pseudopod with assembly at the tip and apparent disassembly at the base. There are no vesicles visible at either the pseudopodial tip or base, so these spermatozoa must have a novel mechanism for insertion and uptake of membrane components. This membrane flow could provide the forward propulsion of spermatozoa attached to a substrate by their pseudopods.

Animals↗
PubMed1981

Composition, stability and electrolyte permeability of Golgi membranes from lactating-rat mammary gland.

1. Golgi membrane vesicles, isolated from lactating-rat mammary gland and greatly enriched in galactosyltransferase (EC 2.4.1.22), contained over 40 separate bands of protein, including some periodic acid)(Schiff-staining material and free thiol groups, when analysed by sodium dodecyl sulphate/polyacrylamide-gel electrophoresis. 2. The membrane lipids were enriched in phosphatidylcholine, phosphatidylethanolamine and unesterified cholesterol. 3. Membrane fluidity, as monitored by the fluorescence polarization of 1,6-diphenylhexa-1,3,5-triene, increased linearly over 5-37 degrees C. 4. The vesicle membranes were impermeable to lactose over a wide pH range, but admitted electrolytes of molecular weight below about 300. 5. These properties are discussed with respect to other cellular membranes and the secretion of milk products.

Animals↗
PubMed1981

Mannitol and glucose movement across the Golgi membrane of lactating-rat mammary gland.

1. Purified Golgi-membrane vesicles of lactating-rat mammary gland were penetrated by glucose. 3-O-methylglucose, mannose, fructose, sorbitol and mannitol, but not by lactose or sucrose. 2. The kinetics of mannitol uptake and release were followed at 2-6 degrees C with the aid of fine filters (0.45 micrometers pore size) to separate the vesicles from the medium. 3. Mannitol efflux exhibited apparent first-order kinetics with k approximately 1 min-1. Neither saturability, nor inhibition by excess sorbitol or glucose, could be observed. 4. Mannitol efflux at 18 degrees C was about seven times faster than at 1 degrees C, and rates at higher temperatures were too fast to be measured. The rate of glucose efflux at 2-6 degrees C exceeded that of mannitol severalfold. 5. These findings imply a channel or carrier of definite, but limited, specificity straddling the Golgi membrane and able to supply glucose for lactose synthesis.

Animals↗
PubMed1981

Sperm morphogenesis in wild-type and fertilization-defective mutants of Caenorhabditis elegans.

Taking advantage of conditions that allow spermatogenesis in vitro, the timing and sequence of morphological changes leading from the primary spermatocyte to the spermatozoon is described by light and electron microscopy. Together with previous studies, this allows a detailed description of the nuclear, cytoplasmic, and membrane changes occurring during spermatozoan morphogenesis. By comparison with wild type, abnormalities in spermatogenesis leading to aberrant infertile spermatozoa are found in six fertilization-defective (fer) mutants. In fer-1 mutant males, spermatids appear normal, but during spermiogenesis membranous organelles (MO) fail to fuse with the sperm plasma membrane and a short, though motile. pseudopod is formed. In fer-2, fer-3, and fer-4 mutants, spermatids accumulate 48-nm tubules around their nuclei where the centriole and an RNA containing perinuclear halo would normally be. In all three mutants, spermatids still activate to spermatozoa with normal fusion of their MOs, but the pseudopods formed are aberrant in most fer-2 and fer-4 spermatozoa and in some fer-3 spermatozoa. In fer-5 mutant males, spermatozoa do not form. Instead, defective spermatids with crystalline inclusions and abnormal internal laminar membranes accumulate. In fer-6 mutant males, only a few spermatozoa form and these have defective pseudopods. These spermatozoa retain their fibrous bodies, a structure which normally disassembles in the spermatid. The time of appearance of developmental abnormalities in all of these mutants correlates with the temperature-sensitive periods for development of infertility. The observation that each of these mutants has a different and discreet set of morphological defects, a structure which normally disassembles in the spermatid. The time of appearance of developmental abnormalities in all of these mutants correlates with the temperature-sensitive periods for development of infertility. The observation that each of these mutants has a different and discreet set of morphological defects, a structure which normally disassembles in the spermatid. The time of appearance of developmental abnormalities in all of these mutants correlates with the temperature-sensitive periods for development of infertility. The observation that each of these mutants has a different and discreet set of morphological defects shows that the strict sequence of morphogenetic events that occurs during wild-type spermatogenesis cannot arise because each event is dependent on previous events. Instead, spermatozoa, like bacteriophages, must be formed by multiple independent pathways of morphogenesis.

Animals↗
PubMed1980

Permeability of lactating-rat mammary gland Golgi membranes to monosaccharides.

The Golgi-membrane vesicles present in particulate preparations of lactating rat mammary gland were biosynthetically loaded with [14C]lactose. This lactose was effectively retained by particles sedimented after exposure to 0.25 M-disaccharide, but was partly lost after exposure to 0.25 M-glucose or other solutes of similar size. Loss of lactose was time-, concentration- and temperature-dependent and varied with the solute structure. This behaviour is ascribed to the presence of protein in the Golgi membrane, forming a specific carrier or channel that serves to supply glucose for lactose synthesis.

Animals↗
PubMed1980

Vesicle fusion, pseudopod extension and amoeboid motility are induced in nematode spermatids by the ionophore monensin.

The sodium- and potassium-transporting ionophore monensin induces the maturation of Caenorhabditis elegans spermatids to spermatozoa in vitro. Rearrangement of cytoplasm, fusion of membranous organelles with the plasma membrane and growth of pseudopodia, all characteristic of in vivo spermiogenesis, occur within five minutes after exposure to monensin at concentrations of 0.1-1.0 micronM. This activation is dependent upon external Na+ and K+ ions but not Ca2+ ions. Monensin-activated spermatozoa have normal morphology and normal amoeboid motility. During activation spermatids twitch and rotate prior to pseudopod extension. Analysis of intermediates by transmission and scanning electron microscopy reveals that the sequence of morphogenetic events leading from the spherical spermatid to the polarized spermatozoan involves microvilli rearrangement and membranous organelle fusion, cytoplasmic polarization, then pseudopod extension.

Animals↗
PubMed1980

Caenorhabditis elegans fertilization-defective mutants with abnormal sperm.

Seven new fertilization-defective mutants of C. elegans have been isolated and characterized; six are temperature sensitive, one is absolute and all are autosomal recessive. One mutation is in a previously described gene, while the other six define six new fer genes that appear to code for sperm-specific functions necessary for normal fertilization. In all fer mutants, both males and hermaphrodites accumulate sperm in near normal numbers. In hermaphrodites, mutant sperm contact the oocytes, but fail to fertilize them. Instead, the sperm are swept into the uterus by the passing oocytes and are expelled when oocytes are laid. Males of two fer mutants do not transfer sperm during copulation, but the other mutant males transfer sperm that fail to move to the spermatheca. Spermatozoa from fer-1 and fer-4 mutants are motility-defective in vitro as well as in vivo, and their pseudopods have an altered morphology. The period of development during which mutant hermaphrodites are temperature sensitive for fertility overlaps the time of sperm development. Some mutants are temperature sensitive throughout the entire period, and others are temperature sensitive during or just prior to spermiogenesis. In fer-4/+ and fer-7/+ males, the fertility of the mutation-bearing sperm is diminished, reducing the transmission ratio. This implies some post-meiotic expression of these genes.--This set of mutants provides a variety of functional and structural alterations in nematode sperm that should help identify and analyze gene products involved in sperm morphogenesis and motility.

Animals↗
PubMed1980

Gonadal dysgenesis in a 46,XY female mosaic for double autosomal trisomies 8 and 21.

The proband was evaluated at 19 years of age because of primary amenorrhoea and, on chromosomal analysis, was found to have a 46,XY karyotype in 75% of her cells and 48,XY, +8, +21 in 25% of her cells. She appeared normal at birth and exhibited normal intellectual and physical development until puberty when secondary sexual differentiation failed. This young women showed none of the dysmorphic features associated with either trisomy 8 or trisomy 21. Her XY gonadal dysgenesis was manifested by late developmental problems of amenorrhoea, sexual infantilism, and gonadal neoplasia.

Adult↗