Determining the genetic basis of reproductive isolation is a fundamental goal in evolutionary biology. Intrinsic reproductive isolation often arises due to epistasis between divergent interacting genes. The rapid evolution of hybrid male sterility is known to have several causes, including the exposure of recessive X-linked incompatibilities in males and the rapid evolution of male reproductive traits. Despite these insights, little is known about the genetics of reproductive isolation during the early stages of speciation. This deficiency inspired parallel studies on the molecular evolution of male reproduction in house mice and the genetic basis of hybrid male sterility between two mouse species, Mus domesticus and M. musculus. Evolutionary analysis of 946 genes showed that the intensity of positive selection varies across sperm development and acts primarily on phenotypes that develop late in spermatogenesis (Appendix A). Several reciprocal crosses between wild-derived strains of M. musculus and M. domesticus were used to examine F1 hybrid male sterility (Appendix B). These crosses revealed hybrid male sterility linked to the M. musculus X chromosome and a novel sterility polymorphism within M. musculus. A large introgression experiment was used to further dissect the genetic basis of X-linked incompatibilities between M. musculus and M. domesticus (Appendix C). Introgression of the M. musculus X chromosome into a M. domesticus genetic background produced male sterility and involved a minimum of four factors. No sterility factors were uncovered on the M. domesticus X chromosome. These data demonstrate the complex genetic basis of hybrid sterility in mice and provide numerous X-linked candidate sterility genes. The molecular evolution of five rapidly evolving candidate genes was examined using population and phylogenetic sampling in Mus (Appendix D). Four of these loci showed evidence of positive natural selection. One locus, 4933436I01Rik, showed divergent protein evolution between M. domesticus and M. musculus and was one of a handful of testis-expressed genes within a narrow interval involved in hybrid male sterility. In summary, these data demonstrate that hybrid male sterility has a complex genetic basis between two closely related species of house mice and provide a foundation for the identification of specific mutations that isolate these species.

Thesis (M.A. ( African languages)) --University of Limpopo, 2013 / The study examines the impact of sterility on Tshivenḓa language and social life. The study deals with words and other linguistic aspects that are generated by this condition and how sterility influences social relations among the Vhavenḓa.

No description available.

High temperature stress (HTS) adversely affects reproduction in most plant species studied to date. HTS during flowering may result in an almost total inhibition of seed production in crop plants. Increasing our knowledge of the effects of HTS on seed production will aid the breeding of more thermotolerant crop plants and improve our understanding of the effects of stress on plants. An investigation of the effects of both drought and high temperature stress on the yields of barley, canola, flax, durum and spring wheat in five locations in Saskatchewan over a 25-year period was performed using multivariate analysis. Higher temperatures during June and July, when the plants were flowering, were correlated with reductions in yields of all the crops studied (except barley in June). A positive correlation between yields and precipitation during May and the winter preceding the growing season was observed.<p>In growth chambers, <i>Brassica napus</i> silique and seed production were inhibited during a ramping HTS treatment. This was due to a decrease in pollen germinability rather than a reduction in the number of flowers produced. HTS also caused reductions in megagametophyte fertility and disrupted embryo and/or seed development.<p>Transgenic plants were developed to overcome the effects of HTS on seed production. Two DNA constructs, one with the <i>Arabidopsis thaliana LEAFY</i> (<i>AtLFY</i>) promoter controlling <i>A. thaliana HEAT SHOCK PROTEIN 101</i> (<i>AtHSP101</i>) ORF expression and another with the <i>AtHSP101</i> promoter controlling <i>AtLFY</i> ORF expression, were inserted into <i>B. napus</i>. Other DNA constructs were made, using the constitutively expressed Cauliflower Mosaic Virus <i>35S</i> or the synthetic <i>EntCup4</i> promoters to control expression of the <i>AtHSP101</i> or <i>A. thaliana HEAT SHOCK TRANSCRIPTION FACTOR 3</i> (<i>AtHSF3</i>) ORFs. These constructs were inserted into both <i>B. napus</i> and <i>A. thaliana</i>. Transgenic plants were tested using a ramping temperature regime but were found not to have increased flower thermotolerance. During the manufacture of the DNA constructs it was determined that, in <i>A. thaliana</i>, 573 bp of <i>AtHSP101</i> had been copied between Terminal Inverted Repeats of a <i>Mu-Like Element</i> (<i>MULE</i>). This fragment was named <i>HSP101B</i>. In some transgenic <i>B. napus</i> and <i>A. thaliana</i> lines, containing 2046 bp of the <i>HSP101B</i> upstream regulatory region controlling <i>B</i>-glucuronidase (GUS) expression, cold-inducible GUS expression was observed. Methylation may have a role in control of endogenous <i>HSP101B</i> transcription.

High temperature stress (HTS) adversely affects reproduction in most plant species studied to date. HTS during flowering may result in an almost total inhibition of seed production in crop plants. Increasing our knowledge of the effects of HTS on seed production will aid the breeding of more thermotolerant crop plants and improve our understanding of the effects of stress on plants. An investigation of the effects of both drought and high temperature stress on the yields of barley, canola, flax, durum and spring wheat in five locations in Saskatchewan over a 25-year period was performed using multivariate analysis. Higher temperatures during June and July, when the plants were flowering, were correlated with reductions in yields of all the crops studied (except barley in June). A positive correlation between yields and precipitation during May and the winter preceding the growing season was observed.<p>In growth chambers, <i>Brassica napus</i> silique and seed production were inhibited during a ramping HTS treatment. This was due to a decrease in pollen germinability rather than a reduction in the number of flowers produced. HTS also caused reductions in megagametophyte fertility and disrupted embryo and/or seed development.<p>Transgenic plants were developed to overcome the effects of HTS on seed production. Two DNA constructs, one with the <i>Arabidopsis thaliana LEAFY</i> (<i>AtLFY</i>) promoter controlling <i>A. thaliana HEAT SHOCK PROTEIN 101</i> (<i>AtHSP101</i>) ORF expression and another with the <i>AtHSP101</i> promoter controlling <i>AtLFY</i> ORF expression, were inserted into <i>B. napus</i>. Other DNA constructs were made, using the constitutively expressed Cauliflower Mosaic Virus <i>35S</i> or the synthetic <i>EntCup4</i> promoters to control expression of the <i>AtHSP101</i> or <i>A. thaliana HEAT SHOCK TRANSCRIPTION FACTOR 3</i> (<i>AtHSF3</i>) ORFs. These constructs were inserted into both <i>B. napus</i> and <i>A. thaliana</i>. Transgenic plants were tested using a ramping temperature regime but were found not to have increased flower thermotolerance. During the manufacture of the DNA constructs it was determined that, in <i>A. thaliana</i>, 573 bp of <i>AtHSP101</i> had been copied between Terminal Inverted Repeats of a <i>Mu-Like Element</i> (<i>MULE</i>). This fragment was named <i>HSP101B</i>. In some transgenic <i>B. napus</i> and <i>A. thaliana</i> lines, containing 2046 bp of the <i>HSP101B</i> upstream regulatory region controlling <i>B</i>-glucuronidase (GUS) expression, cold-inducible GUS expression was observed. Methylation may have a role in control of endogenous <i>HSP101B</i> transcription.

<p>Biodiversity is generated by the process of speciation. Because biological species are defined as populations that are unable to exchange genes with one another, the study of the evolution of reproductive isolation occupies the center of speciation research. A key to deciphering how reproductive isolation evolves is to understand the genetic changes that underlie these barriers to gene flow. Intrinsic postzygotic barriers, such as hybrid sterility or inviability, are known to impede gene flow and especially lend themselves to genetic analysis because of their ease of study in a laboratory setting. Because hybrid sterility likely evolves before hybrid inviability, it potentially plays an important role in the cessation of gene flow. Yet, while their X-linked counterparts have been precisely localized, we remain ignorant of the numbers of and interactions among dominant autosomal loci that are predicted to contribute to F1 hybrid male sterility. </p><p> To address this conceptual void, I examine the genetic architecture of hybrid male sterility between the allopatric sister species Drosophila persimilis and D. pseudoobscura bogotana. First, using a large-scale backcross analysis, I fine-map autosomal QTL from D. persimilis that confer sterility in male hybrids. This fine-mapping shows that loci contributing to hybrid male sterility reside outside chromosomal rearrangements (i.e., regions of reduced recombination) in this allopatric species pairs. In contrast, these QTL do not contribute to hybrid male sterility in the comparable sympatric hybridizing species D. persimilis and D. pseudoobscura, as predicted by models that suggest that hybridizing species persist because of broad regions of reduced recombination. Next, I use a serial backcross design to introgress these sterility-conferring QTL from D. persimilis into a D. p. bogatana genetic background devoid of other alleles from D. persimilis. This introgression study tested a prediction of the dominance theory proposed to explain Haldane's rule: dominant-acting autosomal loci should interact with recessive-acting X-linked loci to produce sterile hybrid males. Surprisingly, the results demonstrated that the "composite" dominance of the autosomal QTL is more important than the dominance of individual QTL for producing Haldane's rule: epistasis among loci elevated their dominant effects on sterility such that individually-recessive-acting autosomal QTL can contribute to F1 male infertility. Finally, using recombination to generate independent lines bearing only small segments of the identified QTL regions, I examine whether single or multiple loci within these regions contribute to the overall effect of hybrid sterility. While the effect of one QTL depends on epistasis between several loci within that small region, the effect of the other QTL appears to derive from a single genetic factor. These results suggest that estimates of the number of genes that contribute to reproductive isolation are at best, likely too low and, at worst, unattainable with the mapping resolution attainable by standard backcross and introgression approaches.</p><p> This dissertation addresses both evolutionary and genetic hypotheses of intrinsic postzygotic isolation. Hybrid male sterility between D. persimilis and D. p. bogotana clearly involves highly specific and complex interactions between homoospecific loci. The mapping results presented here also lay the foundation for the identification and cloning of multiple autosomal sterility-conferring "speciation genes."</p> / Dissertation

Thesis (M.S.)--University of Missouri-Columbia, 2003. / Typescript. Includes bibliographical references (leaves 101-107). Also available on the Internet.

Thesis (M.S.)--University of Missouri-Columbia, 2003. / Typescript. Includes bibliographical references (leaves 101-107). Also available on the Internet.

The cactophilic Drosophila mojavensis species group living in the deserts and dry tropical forests of the Southwestern United States and Mexico provides a valuable system for studies in diversification and speciation. My dissertation addresses a variety of evolutionary genetic questions using this system.Rigorous studies of the relationships between host races of D. mojavensis and the relationships among the members of the species group (D. mojavensis, D. arizona, and D. navojoa) are lacking. I used mitochondrial CO1 sequence data to address the phylogenetics and population genetics of this species group (Appendix A). In this study I have found that the sister species D. mojavensis and D. arizonae share no mitochondrial haplotypes and thus show no evidence for recent introgression. I estimate the divergence time between D. mojavensis and D. arizonae to be between 0.66 and 0.99 million years ago. I performed additional population genetic analyses of these species to provide a basis for future hypothesis testing.In Appendix B, I report the first example of substantial intraspecific polymorphism for genetic factors contributing to hybrid male sterility. I show that the occurrence of hybrid male sterility in crosses between Drosophila mojavensis and its sister species, D. arizonae is controlled by factors present at different frequencies in different populations of D. mojavensis. In addition, I show that hybrid male sterility is a complex phenotype; some hybrid males with motile sperm still cannot sire offspring.The large degree of variation between isofemale lines in producing sterile hybrid sons suggests a complex genetic basis to hybrid male sterility warranting quantitative genetic analysis. Since the genes underlying hybrid male sterility in these species are not yet fixed, I am able to perform explicit genetic analysis of this reproductive isolating mechanism. In Appendix C, I present the results of mapping QTL for hybrid male sterility within species. The genetic architecture underlying hybrid male sterility when analyzed directly in the F1 is highly complex. Thus, hybrid male sterility arises as a complex trait in this system and we propose a drift-based model for the evolution of this phenotype.

Cytoplasmic male sterility (CMS) in plants is associated with mitochondrial dysfunction. We have proposed in this study that the mitochondrial-encoded chimeric peptide thought to be responsible for cytoplasmic male sterility in Polima system could function as a dominant male sterility inducer when expressed in the nucleus and targeted to the mitochondria. Transgenic plants expressing such mitochondrial targeting constructs exhibited reduction of pollen production that was characterized in fertile Westar (nap ) and restored fertile Westar (pol) plants by homeotic transformation of floral organs and in male-sterile Westar (pol) plants by a reduction in pollen production with shortening of the stamens. Genetic and molecular analysis has shown that the phenotypic changes were correlated with the effective genetic transmission of the inserted transgene through female gametes. Most significantly, we have found that differences in floral morphology induced by transgene expression between pol CMS and fertile Westar plants might be related to differences in transcriptional activity of the APETALA3 MADS box gene. We suggest that the alterations in floral morphology that accompany CMS in several plant species might be due to effects of mitochondria on transcriptional activity of floral organ identity genes.