Evolutionary Conservation Genetics explores these exciting avenues of futureresearch potential, integrating ecological quantitative genetics with the new genome science. It is now more important than ever that we ask relevant questions about the evolutionary fate of endangered populations throughout the globe and incorporate our knowledge of evolutionary processes and the distributionof genetic diversity into effective conservation planning and action. Seller Inventory LHB Delivered from our UK warehouse in 4 to 14 business days. Book Description Condition: New. Seller Inventory n.
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Evolutionary Conservation Genetics.
Publisher: Oxford University Press , This specific ISBN edition is currently not available. View all copies of this ISBN edition:. Synopsis About this title Conservation genetics focuses on understanding the role and requirement of genetic variation for population persistence. Alatalo Review : "Those in the fields of ecology, evolutionary biology, and conservation biology will find this book very helpful, as the author explains the often-confusing but central parts of conservation genetics in a straightforward manner.
Unlike the average textbook, however, the author's targeted approach and use of the first person make this text very readable. Because the author assumes basic background knowledge of genetic terms, this text is most appropriate for graduate students or researchers as opposed to undergraduates.
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It would take a probabilistic approach that recognizes the stochasticity inherent in evolutionary change. Dangerous Liaisons? Conservation designation Conservation development Conservation district Conservation easement Ecoregion conservation status Environmental protection Gap analysis Habitat conservation High conservation value area Landscape-scale conservation Marine protected area National conservation area Open space reserve Riparian buffer Roadless area conservation Roadside conservation Site-based conservation Special Area of Conservation. Brassica Crops and Wild Allies. Natural factors, such as storms and diseases, can also cause populations to dwindle. Fecundity, pollen dispersal and mating patterns of roadside Qualea grandiflora Mart.
Evolutionary Conservation Genetics H? Published by OUP Oxford Seller Rating:. New Hardcover Quantity Available: In w females lane 3 , an additional 0. The same primers were used to investigate Dmtra expression patterns in untreated or treated XY; hs- Cctra F1 individuals lanes 5 and 7, respectively. Only a 0. Expression of the CcTRA protein from the transgene does not alter the expression of endogenous Dmtra. Since XY animals are morphologically feminized under the control of transgene-derived CcTRA, we wished to determine the extent to which gonad-genitalia formation is influenced by the presence of the hs- Cctra F1 transgene.
The feminizing activity of hs- Cctra F1 during germline development was analyzed by crossing the strong transgenic lines with Drosophila Dmtra mutant strains. However, analysis of internal genitalia revealed that these individuals either have malformed testes Figure 5c or lack internal genitalia. After heat-shock treatment, a higher percentage of individuals apparently lack germline tissues, but ovarian-like tissues are never formed.
However, the ovarian morphology of germline tissues in XX; hs- Cctra F1; tra females can be rescued after heat induction of the transgene.
Indeed, reinforcement of the transgene activity by heat-shock exposure results in the development of rudimentary or even almost-normal ovaries Figure 5d. Despite the fact that Cctra can support female differentiation of both somatic and germline tissues in XX; tra individuals, these animals fail to lay eggs, thus suggesting that the rescue of the female phenotype is, however, not complete.
A Internal genitalia of hs- Cctra F1 adults after heat-shock treatment. Therefore, we decided to address if the hs- Cctra F1 transgene requires the activity of the endogenous tra2 gene to promote female differentiation.
Accordingly, XX flies carrying a nonfunctional tra2 fail to execute the female program and develop into sterile males F ujihara et al. To this end we introduced the hs- Cctra F1 transgene into a tra2 mutant background. The chromosomes carrying these alleles accumulated recessive lethal mutations and cannot be kept in a homozygous state. Nor could they rescue the tra2 mutant phenotype of the XX mutant flies.
The transformer gene plays a fundamental role in the sex determination of D. Despite its key role in the development of the fly, tra reveals an unusual evolutionary rate even when comparison is restricted to Drosophila species. The evolutionary divergence of this gene becomes even more apparent when a non-drosophilid species, namely C. However, we show here that CcTRA can support not only the somatic, but also the female germline development of Drosophila transgenic strains. A comparison of Ceratitis TRA with homologous proteins from drosophilid species highlighted only a few short regions of identity P ane et al.
In this study, we demonstrate that the function of the TRA protein in Ceratitis and Drosophila is conserved despite the high degree of sequence divergence. Consistently, the expression of an hs- Cctra F1 transgene, encoding the full-length CcTRA protein, in Drosophila transgenic lines drives the female somatic sexual differentiation of otherwise male individuals. Sex transformation affects all somatic tissues and occurs in the strong transgenic lines even in the absence of heat-shock treatment.
A nearly complete somatic sex transformation can also be induced in weak lines after heat-shock exposure, indicating its dependence upon the activity of the hs- Cctra F1 transgene. Indeed, we observe that the expression of a strong hs- Cctra F1 transgene can rescue the ovarian morphology in XX; tra mutant flies.
These flies develop apparently normal ovaries, but upon close inspection, they appear to be sterile and fail to lay eggs. We also observed that ovarian tissues cannot be induced in XY and XY; tra individuals.
This result is rather unexpected, given the positive effect of heat shock on rescue of XX; tra mutants. However, it was previously shown that expression of an hs- Dmtra F transgene is not able to feminize the germline of Drosophila XY individuals M c K eown et al. The absence of ovarian tissues in XY flies might be due to the fact that XY germ cells appear to be less responsive to feminizing signals than XX germ cells W aterbury et al.
In Drosophila, the sexual identity of the developing individual is controlled by tra via the downstream dsx and fru genes. By contrast, in males TRA is not expressed and therefore dsx and fru are spliced in the default male mode. The dsx gene is responsible mainly for the sexual dimorphism of the somatic traits, while fru has been shown to control all aspects of male courtship behavior V illella et al.
In agreement with the sex transformation of Drosophila hs- Cctra F1 transgenic flies, the endogenous dsx and fru genes are expressed in the female mode in the resulting XY pseudofemales. When the TRA-TRA2 complex binds these cis -regulatory elements, it reinforces the usage of suboptimal splicing sites in the dsx and fru primary transcripts and promotes female-specific splicing events T ian and M aniatis Accordingly, XX; tra2 mutants that lack a functional TRA2 protein fail to activate the female processing of dsx and fru and develop as adult pseudomales.
Ccdsx reveals a significant structural and sequence identity when compared to Dmdsx and shows a sex-specific expression pattern S accone et al. The distribution of the cis elements in the Ccdsx gene is also similar to that of Dmdsx , since they are located in exon 4, which is sex-specifically regulated in both Ceratitis and Drosophila S accone et al. Given that CcTRA can promote the proper female splicing of Dmdsx , it is conceivable that it also controls Ccdsx expression using a similar mechanism.
In Ceratitis females, CcTRA is likely to bind the cis elements in Ccdsx exon 4 and to promote the fusion of exon 3 to exon 4. By contrast, in males, where the CcTRA protein is absent, exon 4 is not included in the mature mRNA, with exon 3 being fused directly to exon 5. Consistent with this model, when the Cctra gene is turned off by RNAi in XX individuals, Ccdsx expression pattern is switched from the female to the male mode of splicing P ane et al.
In Ceratitis, Cctra is sex-specifically expressed through post-transcriptional alternative splicing events. Differently, mature mRNAs generated in males retain portions of the intron 1 i. We have reported that the female splicing of the Cctra primary transcripts is dependent upon a functional Cctra gene. These observations lead to the hypothesis that, in Ceratitis females, Cctra controls its own expression by means of a positive feedback loop.
The binding of CcTRA to the cis elements might prevent the usage of male splicing sites, thus leading the splicing machinery to use the criptic female sites. Consequently, intron 1 is removed from Cctra precursor transcripts to produce the female mature mRNAs.
An alternative possibility is represented by an activation mechanism in which CcTRA would enforce the usage of female splice sites. P ane , unpublished results. In this case, the binding of the CcTRA protein to the cis -regulatory elements would favor the use of the female splice sites and promote the removal of the male-specific exons. Both the repression and the activation mechanisms that we propose would involve a new property for the TRA proteins as well as an intronic function for the TRA-TRA2 elements, which has not been described before.
In females, Cctra mature mRNAs have a long open reading frame and represent the source of CcTRA protein to keep the feedback loop active and guarantee the memory of the female sexual state. In males, the M-factor is likely to impair the positive feedback loop at early stages, thus promoting the male developmental program.