The role played by invasive species in interactions with endangered and threatened species in the United States: a systematic review

Invasive species are considered to be a leading cause of the decline of threatened species. However, this view has been disputed because much of the evidence base is anecdotal. This systematic review, through an extensive, repeatable search using agreed selection criteria, examined the available scientific evidence on invasive species’ interactions with the 1363 endangered and threatened species protected under the United States Endangered Species Act (ESA). The review found scientific evidence available for 116 endangered or threatened species (8.5% of the ESA list). Of these, 85 species (6.2%) were reported as being negatively impacted by invasive species: 39 located on the continental US and 39 on islands, with seven marine species. The relative percentages of species impacted differed according to location: 4.3% (n?=?906) on the continental US, 9.3% (n?=?420) on islands. It was found that predation by invasive vertebrates on birds on islands and competition between invasive plants and endangered or threatened plants on the mainland were the main mechanisms of impact. The results of this study contrast markedly with a previous study which found that 49% of imperilled species in the United States were threatened by invasive species. Further research is essential in order to evaluate the impact of invasive species on imperilled species on the ESA list; this would help to reduce the high degree of uncertainty regarding the threat of invasive species due to the lack of empirical information.     

Contribution to the linkage theory of autopolyploids: I

A theory of linkage of autopolyploids is developed under consideration ofm loci andr alleles. The simplifying assumption of chromosome segregation, which may be considered as an approximation to the more adequate theory of chromatid segregation, is made throughout. Random mating and distinct, non-overlapping generations are assumed. Under these assumptions the problem is determined by three basic probability distributions—the distributions of genotypes and of gametes, and the segregation distribution. The segregation distribution is assumed to be the same for males and for females. The aim of the paper is to establish recurrence formulas (which allow to find the distributions of gametes and of genotypes from generation to generation, if the distribution of genotypes for an initial generation is known) and to investigate the limit behavior of these distributions as the number of generations increases indefinitely. In the present paper (hereafter referred to as I) the problem is explained, and the three characteristic distributions are introduced for the general case of a 2s-ploid,m loci, andr alleles. Recurrence relations are established for tetraploids,s=2 andm=2 loci, while the recurrence relations for the general case as well as the limit theorems will be given in the second part of this paper (hereafter referred to as II).     

Contribution to the linkage theory of autopolyploids: II

In the first part of this paper, hereinafter referred to as I, a general segregation, distribution was introduced for autopolyploids (2s-ploids) withm, loci, andr alleles. Random mating, chromosome segragation, distinct generations, and equal segregation distributions for males and females were assumed. In this second part, using this segregation distribution as a basis, a recurrence formula is established which enables us to compute the distribution of gametes for any generation, if this distribution is known for an initial generation. This initial distribution of gametes is derived from the initial distribution of genotypes. The limit behavior of these distributions is completely described in a general limit theorem which contains as particular cases the limit theorems for diploids withm loci, and for 2s-ploids with one locus (Geiringer, 1944, 1945, 1948).     

Standortsuntersuchungen und Neufunde vonHalacsya sendtneri (Boiss.)Dörfl. in Bosnien

Ohne Zusammenfassung     

Stenocereus zopilotensis Arreola-Nava and Terrazas (Cactaceae), a new species from Mexico

Stenocereus zopilotensis Arreola-Nava and Terrazas, a new species from the Zopilote Canyon, municipality of Zumpango del Rio in the center of the state of Guerrero (Mexico), is described and illustrated. This new species is compared toStenocereus quevedonis J. G. Ortega,S. fricii Sánchez-Mej., andS. pruinosus (Otto) Buxb. based on morphological similarity. Moreover, the new species grows sympatrically withS. pruinosus.     

Presence of histone mRNA sequences in high molecular weight RNA of HeLa cells

Pulse-labeled HeLa cell RNA centrifuged under denaturing conditions was hybridized with DNA of recombinant phages containing sea urchin histone genes. This cross-hybridization showed the presence of histone mRNA sequences in high molecular weight RNA molecules. Treatment of the cells with actinomycin to stop RNA synthesis resulted in the rapid decay of this high molecular weight RNA followed by an increase of 9S histone mRNA in the cytoplasm.The results are consistent with the presence in HeLa cells of a high molecular weight precursor to histone messengers.     

Sources of Vibrio mimicus Contamination of Turtle Eggs

Vibrio mimicus contamination of sand increased significantly during the arrival of the olive ridley sea turtles (Lepidochelys olivacea) at Ostional anidation beach, Costa Rica. Statistical analysis supports that eggs are contaminated with V. mimicus by contact with the sand nest. V. mimicus was isolated from eggs of all nests tested, and ctxA⁺ strains were found in 31% of the nests, all of which were near the estuary.     

The H3.3K27M oncohistone affects replication stress outcome and provokes genomic instability in pediatric glioma

While comprehensive molecular profiling of histone H3.3 mutant pediatric high-grade glioma has revealed extensive dysregulation of the chromatin landscape, the exact mechanisms driving tumor formation remain poorly understood. Since H3.3 mutant gliomas also exhibit high levels of copy number alterations, we set out to address if the H3.3K27M oncohistone leads to destabilization of the genome. Hereto, we established a cell culture model allowing inducible H3.3K27M expression and observed an increase in mitotic abnormalities. We also found enhanced interaction of DNA replication factors with H3.3K27M during mitosis, indicating replication defects. Further functional analyses revealed increased genomic instability upon replication stress, as represented by mitotic bulky and ultrafine DNA bridges. This co-occurred with suboptimal 53BP1 nuclear body formation after mitosis in vitro, and in human glioma. Finally, we observed a decrease in ultrafine DNA bridges following deletion of the K27M mutant H3F3A allele in primary high-grade glioma cells. Together, our data uncover a role for H3.3 in DNA replication under stress conditions that is altered by the K27M mutation, promoting genomic instability and potentially glioma development.