Viability analysis of content preparation configurations to deliver 360VR video via MPEG-DASH technology

Abstract Background One of the most challenging tasks in wildlife conservation and management is clarifying which and how external and intrinsic factors influence wildlife demography and long-term viability. The wild population of the Crested Ibis (Nipponia nippon) has recovered to approximately 4400, and several reintroduction programs have been carried out in China, Japan and Korea. Population viability analysis on this endangered species has been limited to the wild population, showing that the long-term population growth is restricted by the carrying capacity and inbreeding. However, gaps in knowledge of the viability of the reintroduced population and its drivers in the release environment impede the identification of the most effective population-level priorities for aiding in species recovery. Methods The field monitoring data were collected from a reintroduced Crested Ibis population in Ningshan, China from 2007 to 2018. An individual-based VORTEX model (Version 10.3.5.0) was used to predict the future viability of the reintroduced population by incorporating adaptive patterns of ibis movement in relation to catastrophe frequency, mortality and sex ratio. Results The reintroduced population in Ningshan County is unlikely to go extinct in the next 50 years. The population size was estimated to be 367, and the population genetic diversity was estimated to be 0.97. Sensitivity analysis showed that population size and extinction probability were dependent on the carrying capacity and sex ratio. The carrying capacity is the main factor accounting for the population size and genetic diversity, while the sex ratio is the primary factor responsible for the population growth trend. Conclusions A viable population of the Crested Ibis can be established according to population viability analysis. Based on our results, conservation management should prioritize a balanced sex ratio, high-quality habitat and low mortality.

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Genetic Control of Recombination Partner Preference in Yeast Meiosis: Isolation and Characterization of Mutants Elevated for Meiotic Unequal Sister-Chromatid Recombination

Genetics ◽

10.1093/genetics/153.2.621 ◽

1999 ◽

Vol 153 (2) ◽

pp. 621-641 ◽

Cited By ~ 10

Author(s):

Dawn A Thompson ◽

Franklin W Stahl

Keyword(s):

Sister Chromatid ◽

Meiotic Recombination ◽

Class Ii ◽

Class Iii ◽

Viability Analysis ◽

Isolation And Characterization ◽

Recombination Checkpoint ◽

Recombination Pathway ◽

Checkpoint Genes ◽

Sister Chromatid Recombination

AbstractMeiotic exchange occurs preferentially between homologous chromatids, in contrast to mitotic recombination, which occurs primarily between sister chromatids. To identify functions that direct meiotic recombination events to homologues, we screened for mutants exhibiting an increase in meiotic unequal sister-chromatid recombination (SCR). The msc (meiotic sister-chromatid recombination) mutants were quantified in spo13 meiosis with respect to meiotic unequal SCR frequency, disome segregation pattern, sporulation frequency, and spore viability. Analysis of the msc mutants according to these criteria defines three classes. Mutants with a class I phenotype identified new alleles of the meiosis-specific genes RED1 and MEK1, the DNA damage checkpoint genes RAD24 and MEC3, and a previously unknown gene, MSC6. The genes RED1, MEK1, RAD24, RAD17, and MEC1 are required for meiotic prophase arrest induced by a dmc1 mutation, which defines a meiotic recombination checkpoint. Meiotic unequal SCR was also elevated in a rad17 mutant. Our observation that meiotic unequal SCR is elevated in meiotic recombination checkpoint mutants suggests that, in addition to their proposed monitoring function, these checkpoint genes function to direct meiotic recombination events to homologues. The mutants in class II, including a dmc1 mutant, confer a dominant meiotic lethal phenotype in diploid SPO13 meiosis in our strain background, and they identify alleles of UBR1, INP52, BUD3, PET122, ELA1, and MSC1-MSC3. These results suggest that DMC1 functions to bias the repair of meiosis-specific double-strand breaks to homologues. We hypothesize that the genes identified by the class II mutants function in or are regulators of the DMC1-promoted interhomologue recombination pathway. Class III mutants may be elevated for rates of both SCR and homologue exchange.

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