Die organischen Kerne der Mammillen in den Frühstadien der Eischalenbildung bei der Lachmöve

Zusammenfassung Lange in Formol gelegene Stücke von Eischalen der Lachmöve (Larus ridibundus) und zwar früheste Stadien ihrer Entwicklung wurden mit Thionin gefärbt und zu Canadabalsampräparaten verarbeitet. In diesen treten die organischen Kerne metachromatisch tingiert hervor, während die Schalenmembran nur einen schwachen bläulichen Ton darbietet. Die Kerne gehen aus den Sekrettropfen hervor, die als erste bei der Schalenbildung aus den tubulösen Uterusdrüsen auf die Schalenmembran gelangen und zu einem Teil in sie eindringen. In Einklang mit den Befunden an Schliffen entspricht der in der Schalenmembran gelegene Teil eines organischen Kernes örtlich dem Bereich des künftigen Eisosphäriten; die nach außen halbkugelig über die Membran vorragende Hälfte aber gehört in den Bereich des künftigen Primärsphäriten mitsamt den konzentrischen Schichten des anstoßenden Kegels. Die organischen Kerne beschränken als Kalkfänger das Ausfallen des Calcits aus dem schalenliefernden Sekret auf bestimmte Stellen der Schalenmembran und legen damit die Orte für die Entstehung der Schalenbausteine (Calcitsphäriten) fest.     

Chronology of permethrin resistance in a southern Illinois population of the horn fly (Diptera: Muscidae) during and after selection by pyrethroid use

From 1985 through 1988, horn flies (Haematobia irritans (L)) collected at the Dixon Springs Agricultural Center (DSAC) in southern Illinois were tested in 22 h bioassays for permethrin resistance with residues on cotton cloths. The LC90 for a susceptible field population collected in June 1985 was 0.19 micrograms/cm2. In comparison, flies collected from pyrethroid-tagged cattle in 1985 and 1986 exhibited 25- to 116-fold resistance to permethrin. A 25-fold level of resistance allowed survival on treated cattle 8 wk after pyrethroid tag application. Flies representing the local background population were collected periodically from an untreated herd 2.4 km from the nearest cattle treated with a pyrethroid; these flies exhibited up to 18-fold resistance. Although pyrethroids were not used on DSAC animals after October 1986, all bioassays done in 1987 and 1988 indicated resistance levels of greater than or equal to 7-fold. The 95% confidence intervals for LC90s from all 1987 bioassays overlapped the confidence interval from the corresponding July 1986 estimate for resistant flies collected from pyrethroid-tagged cattle. Although some decline in resistance was evident in 1988, bioassays done at the end of the season produced resistance ratios of 7.4 and 15.3. Survivorship at a diagnostic dose indicated that resistance frequencies remained at 4-8% throughout 1988. Two years' abstinence from pyrethroid use was insufficient to allow an adequate decline in resistance levels.     

Prolonged incubation with phorbol esters enhanced vasopressin-induced calcium mobilization and polyphosphatidylinositol hydrolysis of vascular smooth muscle cells

Arginine vasopressin (AVP)-induced formation of inositol phosphates and increased calcium efflux in smooth muscle cells (A-10) were inhibited by short term treatment with phorbol 12,13-dibutyrate (PDBu), an activator of protein kinase C (Ca2+/phospholipid-dependent protein kinase) (Aiyar, N., Nambi, P., Whitman, M., Stassen, F. L., and Crooke, S. T. (1987) Mol. Pharmacol. 31, 180-184). Here we report that prolonged treatment of A-10 cells (48 h) with PDBu markedly enhanced AVP-induced calcium mobilization but inhibited ATP- and thrombin-induced calcium mobilization. PDBu (400 nM) doubled [Ca2+]i induced with 3 nM AVP, while the basal calcium concentrations before and after AVP were not different from those of untreated cells. The EC50 for a 24-h exposure was 2.3 nM PDBu. Phorbol 12-myristate 13-acetate was also effective, while 4-alpha-phorbol 12,13-didecanoate (48 h at 400 nM) was without effect. 4-alpha-phorbol 12,13-didecanoate also did not affect inositol phosphate formation. PDBu markedly enhanced inositol phosphate formation induced by AVP but not by NaF. PDBu did not affect basal inositol phosphate and polyphosphoinositide levels, and cytosolic and membrane-associated phospholipase C activity. PDBu treatment (48 h, 400 nM) decreased membrane-associated and cytosolic protein kinase C activity by 80 and 90%, respectively. However, the dose response and time course of changes in protein kinase C activity did not correlate with the same curves for PDBu enhancement of AVP-induced calcium mobilization. We conclude that prolonged PDBu treatment selectively enhanced AVP-induced calcium mobilization and polyphosphoinositide hydrolysis. These effects were not caused by an increase in vasopressin receptor number and apparent affinity, an increase in phospholipase C activity, G-protein-phospholipase C coupling, formation of polyphosphoinositide, or inhibition of inositol phosphate metabolizing enzymes. Enhancement of the AVP responses did not correlate with desensitization or activation of protein kinase C. We suggest that prolonged PDBu treatment might sensitize a putative V1 receptor-G-protein-phospholipase C complex.     

Nucleotide sequence of an OXA-2 beta-lactamase gene from the R-plasmid R1767 derived plasmid pBP11 and comparison to closely related resistance determinants found in R46 and Tn2603

Plasmid pBP11 contains a sequence homologous to Tn21-like element Tn2410 encoding dihydropteroate synthetase and beta-lactamase OXA-2. The nucleotide sequence of a 1.5 kb segment of this region has been determined including the bla gene. It reveals strong sequence homology with the OXA-2 operon of plasmid R46. The implications of an additional 319 bp segment in pBP11 for the different evolution of R46/pKM101 and pBP11 are discussed.     

Biosynthesis of digalactosyldiacylglycerol in plastids from 16:3 and 18:3 plants

Intact chloroplasts isolated from leaves of eight species of 16:3 and 18:3 plants and chromoplasts isolated from Narcissus pseudonarcissus L. flowers synthesize galactose-labeled mono-, di-, and trigalactosyldiacylglycerol (MGDG, DGDG, and TGDG) when incubated with UDP-[6-³H]galactose. In all plastids, galactolipid synthesis, and especially synthesis of DGDG and TGDG, is reduced by treatment of the organelles with the nonpenetrating protease thermolysin. Envelope membranes isolated from thermolysin-treated chloroplasts of Spinacia oleracea L. (16:3 plant) and Pisum sativum L. (18:3 plant) or membranes isolated from thermolysin-treated chromoplasts are strongly reduced in galactolipid:galactolipid galactosyltransferase activity, but not with regard to UDP-Gal:diacylglycerol galactosyltransferase. For the intact plastids, this indicates that thermolysin treatment specifically blocks DGDG (and TGDG) synthesis, whereas MGDG synthesis is not affected. Neither in chloroplast nor in chromoplast membranes is DGDG synthesis stimulated by UDP-Gal. DGDG synthesis in S. oleracea chloroplasts is not stimulated by nucleoside 5′-diphospho digalactosides. Therefore, galactolipid:galactolipid galactosyltransferase is so far the only detectable enzyme synthesizing DGDG. These results conclusively suggest that the latter enzyme is located in the outer envelope membrane of different types of plastids and has a general function in DGDG synthesis, both in 16:3 and 18:3 plants.     

A cyclic AMP response element mediates repression of tyrosine aminotransferase gene transcription by the tissue-specific extinguisher locus Tse-1

Tyrosine aminotransferase (TAT) gene expression is liver specific and inducible by glucocorticoids and via the cAMP signaling pathway. In fibroblasts and other nonliver cells the gene is subject to negative control by the trans-dominant tissue-specific extinguisher locus Tse-1. We identified a hepatocyte-specific enhancer that is repressed by Tse-1. Two distinct sequence motifs are absolutely essential for function of this enhancer: a cAMP response element (CRE), which is the target for repression by Tse-1, and a hepatocyte-specific element. The specificity of the enhancer is generated by the combination of these two essential elements, which are fully interdependent. In vivo footprinting indicates that Tse-1 acts by affecting protein binding at the CRE. A direct antagonism between Tse-1 and the cAMP signaling pathway suggests that Tse-1 plays a role in control of developmental activation of the TAT gene.     

The rate of bulk flow from the Golgi to the plasma membrane

A truncated analog of the backbone of sphingomyelin and glycolipids was synthesized. This truncated C8C8 ceramide was soluble in water (but was still able to cross cell membranes) and was utilized by the Golgi apparatus of living cells to produce water-soluble truncated phospholipids and glycolipids that were then secreted into the medium. Sphingomyelin is synthesized in a proximal (likely the cis) Golgi compartment. At 37 degrees C in CHO cells, the sphingomyelin analog is secreted with a half time of about 10 min. With this rate of bulk flow, no special signal is needed to pass through the Golgi to the plasma membrane. At 30 degrees C the half time of secretion of a lumenal ER marker is about 18 min, and that of the truncated sphingomyelin is about 14 min. Comparison of these rates sets an upper limit of about 4 min for half of the ER to be drained into the proximal Golgi at 30 degrees C.