Species turnover of corticolous bryophyte assemblages over 15 years in an Australian subtropical cloud forest

Montane forest ecosystem characterized by frequent cloud or mist inundation are considered highly vulnerable to climatic change. Despite this, there is a paucity of long‐term studies assessing community change within these important ecosystems. We present the first comparative analysis of corticolous bryophyte diversity over 15 years in high elevation forests of the Gondwana Rainforests of Australia World Heritage Area, south‐east Queensland, Australia. We found limited evidence of change in species richness across the five isolated stands of microphyll fern forest studied. However, we document considerable species turnover within corticolous bryophyte communities with a large and coherent pattern of change in the liverwort flora in particular (43–62% species turnover). Liverworts, but not mosses, also exhibited strong spatial patterns in species assemblages that likely correspond to varying exposure to orographic moisture associated with south‐easterly winds. We postulate that microclimatic factors are stronger determinants of liverwort assemblages than moss assemblages in this system and that documented directional change in liverwort communities is a response to temporal fluctuation in moisture inputs from orographic cloud that are not discernible from precipitation records.     

Major histocompatibility complex class II polymorphisms in humans and chimpanzees

Allelic variation at the MhcPatr-DR and -DQ loci was studied by molecular biological techniques and compared to available HLA data. With regard to the number of allelic lineages, the chimpanzee shows a condensation of its major histocompatibility complex (MHC) class II repertoire as compared to humans. This does not have an impact on the overall degree of MHC class II polymorphism in the chimpanzee since a few lineages that are oligomorphic in humans display an extensive degree of polymorphism in the chimpanzee.     

Defining the locus of origin of a genetically determined electrophoretic variant of a multilocus enzyme system; the calcutta-1 of human LDH system is a B-locus variant

Summary Six (four Hindus, one Sikh, and one Muslim) out of 213 individuals originating from different parts of the Indian subcontinent (namely, Andhra Pradesh, Maharashtra, Uttar Pradesh, East Punjab, and West Punjab) were found to be Calcutta-1 (CAL1) variants of lactate dehydrogenase (LDH). The CAL1 variant was originally described (and thus, generally believed at present) as an allelic variant at the LDHA locus in chromosome 11. By using an improved Cellogel electrophoretic procedure the isozyme patterns observed in the erythrocytes and leukocytes of the variant have indicated that the CAL1 is not a variant of LDHA but that of LDHB, a chromosome 12 marker. This suggestion was supported by the isozyme patterns of LDH in a set of segregating clones of man-mouse somatic cell hybrids with the variant as human partner. Moreover, the variant cosegregated consistently with the human chromosome 12 and with the markers firmly assigned to the latter but not with human chromosome 11 or its markers in these hybrids. These results confirmed that the CAL1 is an LDHB variant.     

Cardiac lipoprotein lipase: effects of lipopolysaccharide and tumor necrosis factor

Summary Lipopolysaccharide (LPS), the active principle of certain endotoxins, protein-free perfused in rat hearts leads in 3 h to a considerable loss of lipoprotein lipase (LPL) activity. In the presence of albumin LPS has virtually no effect. Tumor necrosis factor (TNF) added instead of LPS had no effects on LPL activity during 3 hin vitro perfusion. LPS injected into rats intravenously leads within 3 h to severe toxic phenomena amongst which increased capillary permeability. This was visualized as increased rate of interstitial fluid formation in Langendorff hearts mounted 3 h after rats had been treated with LPS. LPL activity did not decline in 3 h lasting endotoxemia. Six hours after LPS injection, however, cardiac LPL activity was considerably lowered, although immunoblotting and immunohistochemistry still showed LPL protein to be present. These date indicate the presence of a considerable pool of inactive LPL protein in addition to active LPL, that can be released in the presence of heparin. The LPL activity is lowered by LPS injection after a lag phase of at least 3 h, while capillary endothelial cells are influenced more rapidly. The relatively late expression of TNF toxicity in cardiomyocytes of the intact heart is discussed.     

Fibroblast dedifferentiation as a determinant of successful regeneration

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Molecular mechanisms involved in the production of cromosomal aberrations II. Utilization of neurospora endonuclease for the study of aberration production by X-rays in G1 and G2 stages of the cell cycle

Chinese hamster ovary cells (CHO) were X-irradiated in G₁ and G₂ stages of the cell cycle and subsequently Neurospora endonuclease (NE) (E.C.3.1.4), an enzyme which is specific in cleaving single-stranded DNA, was introduced into the cells, after making the cells permeable by treatment with inactivated Sendai virus. With this treatment all classes of X-ray-induced chromatid aberrations increased in G₂ cells, whereas in G₁ cells an increase in cromosome type of aberrations was found, associated with a profound induction of chromatid type of aberrations as well. Duration of the availability of single-strand gaps for the action of NE has been studied in G₂ cells following X-irradiation and the influence of different parts of the G₂ stage on the type and frequencies of chromatid aberrations was discerned. While the increase in chromosome type of aberrations by NE in X-irradiated G₁ cells has been interpreted as due to the conversion of DNA single-strand breaks or gaps to double-strand breaks by NE, the induction of chromatid aberrations in G₁ has been assumed to be due to conversion of some of the damaged bases strand breaks by NE. Biochemical evidence is presented for the conversion by NE of DNA single-strand breaks induced by X-rays into double-strand breaks using neutral sucrose gradient centrifugation.     

Mhc-DQB repertoire variation in hominoid and Old World primate species.

Comparison of 87 distinct Mhc-DQB sequences, obtained from 13 primate species, demonstrates that five out of eight trans-species Mhc-DQB allele lineages are at least 30 million years old and predate divergence of hominoid and Old World primate species. One lineage may be much older because its members are not only traced back in higher primates, but also are present in a New World primate species. Comparing Mhc-DQB repertoire variation in distinct species, allows one to pinpoint when certain polymorphisms were lost or gained in primate evolution. Heterogeneity observed among members of trans-species Mhc-DQB allele lineages can be explained in major part by point mutations, whereas intraexonic crossing-over is a potent mechanism in generating new allele lineages. The stability of Mhc-DQB polymorphisms is influenced by selective forces because distinct allele lineages appear to have accumulated nucleotide substitutions and amino acid replacements at different rates.     

A personal computer program for large-scale comparisons of related nucleotide sequences

A personal computer program (COMPSEQ) has been developed whichcan present an informative listing of pre-aligned exonic nucleotidesequences and of their translations to amino acid sequencesas well run triplet-oriented analyses on these sequences ina given reading frame. The sequence listing focuses on the differencesbetween related sequences by suppressing the concordances betweenthem.     

Endothelial nitric oxide synthase and its negative regulator caveolin-1 localize to distinct perinuclear organelles.

Caveolin-1 is a member of a subset of intracellular proteins that regulate endothelial nitric oxide synthase (eNOS) activity. In caveolae, caveolin-1 inhibits eNOS activity via a direct interaction with the enzyme. Previous work has indicated that both eNOS and caveolin-1 are also localized at the perinuclear Golgi complex. Whether caveolin-1 is involved in eNOS regulation in this cell compartment is unknown. Here we studied the localization of eNOS and caveolin-1 in the perinuclear region of primary bovine aortic endothelial cells. By immunofluorescence microscopy we show that both eNOS and caveolin-1 co-localize with Golgi markers. On treatment of the cells with the microtubule-depolymerizing drug nocodazole, the Golgi complex is scattered and caveolin-1 is found in vesicles at the periphery of the cell, while eNOS is localized at large structures near the nucleus. The nocodazole-induced redistribution of eNOS is similar to that of cis-, medial-, and trans-Golgi markers, while the caveolin-1 redistribution resembles that of sec22, a marker for the intermediate compartment. The localization of eNOS and caveolin-1 at distinct perinuclear compartments that behave differently in the presence of nocodazole indicates that eNOS activity is not regulated by caveolin-1 in the Golgi complex.