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S Strome

Publications and source records attributed to S Strome.

52 records · Page 3Linked to original sources
PubMed1989

A sperm-supplied product essential for initiation of normal embryogenesis in Caenorhabditis elegans is encoded by the paternal-effect embryonic-lethal gene, spe-11.

Loss-of-function mutations in the spe-11 gene in Caenorhabditis elegans result in a paternal-effect embryonic-lethal phenotype: fertilization of wild-type oocytes by sperm from homozygous spe-11 mutant males leads to abnormal zygotic development, whereas oocytes from homozygous spe-11 hermaphrodites when fertilized by wild-type sperm develop normally. Embryos fertilized by sperm from homozygous spe-11 worms fail to complete meiosis and show defects in eggshell formation, mitotic spindle orientation, and cytokinesis. Genetic analysis suggests that the spe-11 gene is expressed before the completion of spermatogenesis and that the wild-type locus encodes a product that is present in sperm and participates, directly or indirectly, in initiating the correct program of early events in C. elegans embryos. Such an ontogenetic role of the spe-11+ gene product in early embryogenesis distinguishes spe-11 mutations from the two paternal-effect mutations identified in Drosophila, ms(3)K81 and pal, which primarily affect chromosome behavior. Analysis of spe-11 provides the first step toward genetic dissection of the functions of the sperm in early embryogenesis in C. elegans.

Animals↗
PubMed1989

Generation of cell diversity during early embryogenesis in the nematode Caenorhabditis elegans.

Caenorhabditis elegans zygotes undergo a series of four differentiative divisions to generate 5 somatic founder cells and a germ-line progenitor cell by the 16- to 24-cell stage of embryogenesis. The pattern of divisions, cell positions, and development of the embryonic cells are invariant from embryo to embryo. Through a combination of embryo manipulation, treatment of embryos with pharmacologic agents, and genetic analysis of maternal-effect embryonic-lethal mutants, researchers in several laboratories have investigated when and how cell differences are generated and cell fates are specified during embryogenesis: 1. Most blastomeres develop in a cell-autonomous manner. They do not need to undergo cell division and they do not require their normal neighbors to express differentiation products characteristic of their lineage. In embryos in which specific cells have been ablated, the fates of neighboring cells do not change to compensate for the missing cells. These observations suggest that most embryonic cells are determined by lineally transmitted internally segregated information. 2. There is at least one clear-cut example of inductive interactions during early development. The anterior daughter of AB gives rise to hypodermis, neurons, pharyngeal muscles, and body wall muscles. Interactions between ABa cells and P1-derived blastomeres are required between the 4- and 28-cell stage for ABa to generate pharyngeal and body wall muscles. ABa appears to be directed to generate hypodermis by internally segregated cues and directed to generate muscle by external cues. 3. Certain of the early internal segregation events require the participation of microfilaments. Disruption of the microfilament array leads to the missegregation of germ granules and of the potential of cells to undergo unequal germ-line-like divisions. Microfilaments may be involved in many other segregation events as well. 4. Several maternal-effect lethal mutants also perturb zygotic segregation events. These par mutants, which divide symmetrically and fail to segregate germ granules, may identify genes whose products interact with microfilaments or otherwise participate in cytoplasmic localization during the early divisions.

Animals↗
PubMed1988

An analysis of the role of microfilaments in the establishment and maintenance of asymmetry in Caenorhabditis elegans zygotes.

Microfilaments are needed to generate asymmetry during the first cell cycle in Caenorhabditis elegans zygotes. To investigate when and how microfilaments participate in this process, we have "pulsed" zygotes with the microfilament inhibitor cytochalasin D (CD) at different times during the cell cycle. We have shown that microfilaments are only required during a narrow time interval approximately three-quarters of the way through the first cell cycle for the manifestations of asymmetry that occur during and subsequent to this interval. When CD treatment spans this critical time interval, pseudocleavage, pronuclear migration, germ-granule segregation (all of which occur during the interval), and movement of the mitotic spindle to an asymmetric position (which occurs later in the cell cycle) are perturbed. In contrast, embryos briefly treated with CD before or after the critical time interval manifest normal asymmetry. Our results suggest that in C. elegans microfilaments participate in the generation of zygotic asymmetry by providing spatial cues and/or serving as a part of the necessary machinery only during a brief period in the first cell cycle, and are not required to maintain asymmetries that have already been established.

Actin Cytoskeleton↗
PubMed1987

Geriatric assessment on a subacute hospital ward.

The authors collected data on all patients admitted to the Sepulveda Veterans Administration Geriatric Evaluation Unit (GEU) during its first 6 years of operation. Analysis of these data indicate several beneficial effects associated with this type of specialized geriatric care: improved diagnostic accuracy, reduced use of drugs, improved functional status, and improved placement location. The authors also analyzed additional data from a previously published, randomized controlled trial to compare better process of care between patients randomized to the GEU and those receiving usual services. During their initial hospitalizations, GEU patients received significantly more specialty evaluations than controls (4.9 versus 1.7, p less than .001), had longer lengths of stay (85.1 days versus 44.3 days, p less than .001), had more new diagnoses discovered (2.9 versus 0.6, p less than .001), and had more drugs discontinued from their regimens (4.6 versus 2.3 p less than .001). These process differences were probably related to the previously reported outcome differences: GEU patients were more likely than controls to show improvements in functional status, affect, placement location, use of institutional services, and survival.

Aged↗
PubMed1986

Monoclonal antibodies that recognize a polypeptide antigenic determinant shared by multiple Caenorhabditis elegans sperm-specific proteins.

Four monoclonal antibodies that are directed against antigens present in sperm and absent from other worm tissues were characterized. Antibody TR20 is directed against the major sperm proteins, a family of small, abundant, cytoplasmic proteins that have been previously described (Klass, M. R., and D. Hirsh, 1981, Dev. Biol., 84:299-312; Burke, D. J., and S. Ward, 1983, J. Mol. Biol., 171:1-29). Three other antibodies, SP56, SP150, and TR11, are all directed against the same set of minor sperm polypeptides that range in size from 29 to 215 kD. More than eight different sperm polypeptides are antigenic by both immunotransfer and immunoprecipitation assays. The three antibodies are different immunoglobulin subclasses, yet they compete with each other for antigen binding so they are directed against the same antigenic determinant on the multiple sperm proteins. This antigenic determinant is sensitive to any of six different proteases, is insensitive to periodate oxidation or N-glycanase digestion, and is detectable on a polypeptide synthesized in vitro. Therefore, the antigenic determinant resides in the polypeptide chain. However, peptide fragments of the proteins are not antigenic, thus the determinant is likely to be dependent on polypeptide conformation. The antigenic determinant shared by these proteins could represent a common structural feature of importance to the localization or cellular specificity of these proteins.

Animals↗
PubMed1986

Fluorescence visualization of the distribution of microfilaments in gonads and early embryos of the nematode Caenorhabditis elegans.

Several intracellular motility events in the Caenorhabditis elegans zygote (pseudocleavage, the asymmetric meeting of the pronuclei, the segregation of germ line-specific granules, and the generation of an asymmetric spindle) appear to depend on microfilaments (MFs). To investigate how MFs participate in these manifestations of zygotic asymmetry, the distribution of MFs in oocytes and early embryos was examined, using both antibodies to actin and the F-actin-specific probe rhodamine-phalloidin. In early-stage zygotes, MFs are found in a uniform cortical meshwork of fine fibers and dots or foci. In later zygotes, concomitant with the intracellular movements that are thought to be MF mediated, MFs also become asymmetrically rearranged; as the zygote undergoes pseudocleavage and as the germ line granules become localized in the posterior half of the cell, the foci of actin become progressively more concentrated in the anterior hemisphere. The foci remain anterior as the spindle becomes asymmetric and the zygote undergoes its first mitosis, at which time fibers align circumferentially around the zygote where the cleavage furrow will form. A model for how the anterior foci of actin may participate in zygotic motility events is discussed. Phalloidin and anti-actin antibodies have also been used to visualize MFs in the somatic tissues of the adult gonad. The myoepithelial cells that surround maturing oocytes are visibly contractile and contain an unusual array of MF bundles; the MFs run roughly longitudinally from the loop of the gonad to the spermatheca. Myosin thick filaments are distributed along the MFs in a periodic manner suggestive of a sarcomere-like configuration. It is proposed that these actin and myosin filaments interact to cause sheath cell contraction and the movement of oocytes through the gonad.

Actin Cytoskeleton↗
PubMed1983

Generation of asymmetry and segregation of germ-line granules in early C. elegans embryos.

Germ-line granules in C. elegans embryos (P granules) can be visualized by immunofluorescence microscopy using a monoclonal antibody. In mutant zygotes with abnormal spindle orientations and in wild-type zygotes treated with the microtubule inhibitors nocodazole, colcemid, vinblastine, and griseofulvin, both P-granule segregation to the posterior pole and the concomitant pseudocleavage occur apparently normally, but the normally concurrent migration of the pronuclei is inhibited. Conversely, treatment of wild-type embryos with the microfilament inhibitors cytochalasins D and B inhibits P-granule segregation and pseudocleavage, as well as other manifestations of polarity, without preventing pronuclear migration. The results suggest that P-granule segregation does not require either the spindle or cytoplasmic microtubules, but that this process as well as generation of other asymmetries does require cytoskeletal functions that depend on microfilaments.

Animals↗
PubMed1982

Immunofluorescence visualization of germ-line-specific cytoplasmic granules in embryos, larvae, and adults of Caenorhabditis elegans.

By using fluorescent antibody staining, we have followed cytoplasmic granules unique to germ-line cells throughout the life cycle of Caenorhabditis elegans. These elements, designated P granules, are segregated exclusively to germ-line precursor cells during early embryogenesis. Prior to mitosis at each of the early cleavages that produce a somatic and germ-line daughter cell, the granules become localized in the region of cytoplasm destined for the germ-line daughter. After the 16-cell stage, the granules appear to be associated with the nuclear envelope. P granules persist in the germ cells throughout the larval and adult stages. The P granules are similar in number, size, and distribution to germ-line-specific structures identified as "germinal plasm" by electron microscopy in C. elegans embryos.

Animals↗
PubMed1982

Elevation of serum angiotensin-converting enzyme level. Occurrence in alcoholic liver disease.

Serum angiotensin-converting enzyme (ACE) levels were measured in 151 patients with chronic alcoholism and alcoholic liver disease. The mean serum ACE level was elevated to 30.8 +/- 13 units/mL compared with 22.8 +/- 6 units/mL in control subjects. Approximately 30.0% of the patients had elevated ACE levels. Abstinence from alcohol for six to 27 months by 11 patients was associated with persistently normal serum ACE levels. Angiotensin-converting enzyme level elevations did not correlate with abnormalities of other liver function test results or with any acute clinical condition associated with alcoholic cirrhosis. Hypoxemia was not present in the patients with elevated serum ACE levels. Elevations of serum ACE levels in patients with alcoholic liver disease may relate to an effect of alcohol on the hepatic-sinusoidal lining cells. This elevation could interfere with the use of this test for supporting the diagnosis of sarcoidosis.

Alcohol Drinking↗
PubMed1981

Continued heavy drinking and survival in alcoholic cirrhotics.

Survival of 64 male chronic alcoholic cirrhotics with first-onset ascites discharged from a gastrointestinal convalescent service was examined over a 32-mo period of study. Of 54 patients discharged as improved, 23 (43%) remained abstinent for a mean time of 14.0 mo and 15 (28%) resumed heavy drinking (greater than 2 g/kg/day). Twelve of 15 heavy drinkers died in a mean time of 7.2 mo, while all but one abstainer were alive. Differences in survival were statistically significantly different (p less than 0.001) when examined by the life-table method. Survival of 16 "moderate or binge" drinkers was not significantly different from abstainers. However, the number of rehospitalizations for liver disease was increased in this group. The study indicates that continued heavy drinking is associated with poor survival of alcoholic cirrhotics.

Adult↗