Worldwide distribution of commercial resources of seaweeds including Gelidium

The commercial exploitation of seaweeds for use as food and for the production of agar, alginate and carrageenan is outlined. The quantities of seaweed harvested for each purpose are tabulated and discussed. Seaweeds for food are derived chiefly from China, Japan and Korea, with almost 94% obtained by cultivation. Alginophytes are collected in 15 countries but six of these account for more than 80% of the total harvest; all are from natural stocks except for a large quantity of Laminaria cultivated in China. Natural carrageenophytes, from 12 countries, now account for only 20% of the total harvest; the remainder is cultivated Eucheuma species, 99% of which is produced in only two countries, the Philippines and Indonesia. Of the four categories of commercial resources of seaweeds considered, agarophytes are spread more evenly over a greater number of countries; they come from 20 countries and only five of these are minor contributors to the total. Gelidium species are particularly important because of the high quality agar they yield; their distribution and location are discussed.     

Degradation of HeLa S3 cell chromatin by auromomycin and its chromophore

The antitumor protein agent auromomycin was found to degrade chromatin structure primarily by inducing strand scissions in linker regions. The reaction was stimulated by dithiothreitol. The chromophore form of the drug caused similar effects on chromatin, but it appeared to function at a more rapid rate. There was no evidence that auromomycin could cause breakage in core regions of chromatin.     

Bizelesin, a bifunctional cyclopropylpyrroloindole alkylating agent, inhibits simian virus 40 replication in trans by induction of an inhibitor.

Bizelesin, a bifunctional DNA minor groove alkylating agent, inhibits both cellular and viral (SV40) DNA replication in whole cells. Bizelesin inhibition of SV40 DNA replication was analyzed in SV40-infected cells, using two-dimensional (2D) neutral agarose gel electrophoresis, and in a cell-free SV40 DNA replication assay. Within 1 h of bizelesin addition to infected cells, a similar rapid decrease in both the level of SV40 replication intermediates and replication activity was observed, indicating inhibition of initiation of SV40 DNA replication. However, prolonged bizelesin treatment (>/=2 h) was associated with a reduced extent of elongation of SV40 replicons, as well as the appearance on 2D gels of intense spots, suggestive of replication pause sites. Inhibition of elongation and induction of replication pause sites may result from the formation of bizelesin covalent bonds on replicating SV40 molecules. The level of in vitro replication of SV40 DNA also was reduced when extracts from bizelesin-treated HeLa cells were used. This effect was not dependent upon the formation of bizelesin covalent bonds with the template DNA. Mixing experiments, using extracts from control and bizelesin-treated cells, indicated that reduced DNA replication competence was due to the presence of a trans-acting DNA replication inhibitor, rather than to decreased levels or inactivation of essential replication factor(s).     

Increased catalytic activity of cytochrome P-450IIE1 in pericentral hepatocytes compared to periportal hepatocytes isolated from pyrazole-treated rats.

Cytochrome P-450IIE1 is induced by a variety of agents, including acetone, ethanol and pyrazole. Recent studies employing immunohistochemical methods have shown that P-450IIE1 was expressed primarily in the pericentral zone of the liver. In order to evaluate whether catalytic activity of P-450IIE1 is preferentially localized in the pericentral zone of the liver acinus, the oxidation of aniline and p-nitrophenol, two effective substrates for P-450IIE1, by periportal and pericentral hepatocytes isolated from pyrazole-treated rats was determined. Periportal and pericentral hepatocytes were prepared by a digitonin-collagenase procedure; the marker enzymes glutamine synthetase and gamma-glutamyl transpeptidase indicated reasonable separation of the two cell populations. Viability, yield and total cytochrome P-450 content were similar for the periportal and pericentral hepatocytes. Pericentral hepatocytes oxidized aniline and p-nitrophenol at rates that were 2-4-fold greater than periportal hepatocytes under a variety of conditions. Carbon monoxide inhibited the oxidation of the substrates with both preparations and abolished the increased oxidation found with the pericentral hepatocytes. Pyrazole or 4-methylpyrazole, added in vitro, effectively inhibited the oxidation of aniline and p-nitrophenol and prevented the augmented rate of oxidation by the pericentral hepatocytes. Western blots carried out using isolated microsomes revealed a more than 2-fold increase in immunochemical staining with microsomes isolated from the pericentral hepatocytes, which correlated to the 2-4-fold increase in the rate of oxidation of aniline or p-nitrophenol by the pericentral hepatocytes. These results suggest that functional catalytic activity of cytochrome P-450IIE1 is preferentially localized in the pericentral zone of the liver acinus, and that most of the induction by pyrazole of P-450IIE1 appears to occur within the pericentral zone.     

A comprehensive analysis of the developmental and tissue-specific expression of the isoactin multigene family in the rat.

The present study represents the first comprehensive analysis of isoactin gene expression in the developing rat. Our results clearly demonstrate that the developmental and tissue-specific expression of the actin multigene family is a highly integrated and complex process involving a variety of regulatory paradigms. The distinct temporal patterns of expression reported in this study indicate that there are three key phases in the regulation of expression of the actin multigene family during development. These include early embryonic development, late fetal development, and early postnatal development. The specific spatial patterns of expression observed in this study demonstrate that the expression of the actin multigene family is much more permissive than previously reported. This permissive expression includes a wide range of "ectopic" expression of the striated muscle isoactins as well as an extended expression of the alpha-smooth muscle isoactin. These findings expand our current understanding of the expression of the actin multigene family in development and provide a fundamental basis for future studies directed at investigating these processes.     

Co-invasion of three Asian earthworms, <Emphasis Type="Italic">Metaphire hilgendorfi</Emphasis>, <Emphasis Type="Italic">Amynthas agrestis</Emphasis> and <Emphasis Type="Italic">Amynthas tokioensis</Emphasis> in the USA

Earthworm invasions are one of the most serious causes of ecological deterioration in the temperate deciduous forests of North America. Non-native earthworms impact understory vegetation, leaf litter layer, carbon dynamics, nutrient availability, and the associated food webs. Here we report a significant status change and confirm expansion of known range of Amynthas agrestis, one of the most serious invasive species in North America, and two of its close relatives, A. tokioensis and Metaphire hilgendorfi. The three species have never been confirmed to co-occur in North American ecosystems. We examined 1760 earthworms collected from 30 sites across northeastern USA, and identified them using a new morphological key. Our data show that sympatric occurrence of at least two, and often all three, species is more common than having only one species. In addition, A. tokioensis was dominant in many of these earthworm communities. The status change in species composition from only one species to two or three and the shift in dominance are most likely caused by previous incorrect species identification. Our results support expansion of known range of A. tokioensis and M. hilgendorfi northward and westward into states with colder winters. This range expansion may have taken place alongside that of A. agrestis in the last 10–20 years, but has long been overlooked. Altogether, results highlight an urgent need for correct species identification. The recognition of an expanding multi-species system represents a unique opportunity to further evaluate complex interactions among co-invading and resident species, and to investigate whether interspecific interactions have unexpected non-additive impacts on ecological processes.     

Novel reagents for chemical cleavage at abasic sites and UV photoproducts in DNA.

Hot piperidine is often used to cleave abasic and UV-irradiated DNA at the sites of damage. It can inflict non-specific damage on DNA, probably because it is a strong base and creates significant concentrations of hydroxyl ions which can attack purines and pyrimidines. We show that several other amines can cleave abasic DNA at or near neutral pH without non-specific damage. One diamine, N,N'-dimethylethylenediamine, efficiently cleaves abasic DNA at pH 7.4 by either beta- or beta,delta-elimination, depending on temperature. Using end-labelled oligonucleotides we show that cleavage depends mainly on elimination reactions, but that 4',5'-cyclization is also significant. This reagent also cleaves at photoproducts induced by UVC and UVB, producing the same overall pattern as piperidine, but with no non-specific damage. It should prove valuable in locating low levels of photoproducts in DNA, such as those induced by natural sunlight.     

A high-resolution linkage map of the lethal spotting locus: a mouse model for Hirschsprung disease

Mice homozygous for the lethal spotting (ls) mutation exhibit aganglionic megacolon and a white spotted coat owing to a lack of neural crest-derived enteric ganglia and melanocytes. The ls mutation disrupts the migration, differentiation, or survival of these neural crest lineages during mammalian development. A human congenital disorder, Hirschsprung disease (HSCR), is also characterized by aganglionic megacolon of the distal bowel and can be accompanied by hypopigmentation of the skin. HSCR has been attrrbuted to multiple loci acting independently or in combination. The ls mouse serves as one animal model for HSCR, and the ls gene may represent one of the loci responsible for some cases of HSCR in humans. This study uses 753 N₂ progeny from a combination of three intersubspecific backcrosses to define the molecular genetic linkage map of the ls region and to provide resources necessary for positional cloning. Similar to some cases of HSCR, the ls mutation acts semidominantly, its phenotypic effects dependent upon the presence of modifier genes segregating in the crosses. We have now localized the ls mutation to a 0.8-cM region between the D2Mit113 and D2Mit73/D2Mit174 loci. Three genes, endothelin-3 (Edn3), guanine nucleotide-binding protein -stimulating polypeptide 1 (Gnas), and phosphoenolpyruvate carboxykinase (Pck1) were assessed as candidates for the ls mutation. Only Edn3 and Gnas did not recombine with the ls mutation. Mutational analysis of the Edn3 and Gnas genes will determine whether either gene is responsible for the neural crest deficiencies observed in ls/ls mice.Both authors contributed equally to this research.