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Species interactions, by changing phenotypic traits, can alter the outcome of subsequent interactions. Plant-mediated responses to herbivores have been extensively studied, but little is known about plant-mediated responses involving parasitic plants within a broader community context that also includes herbivores. Because parasitic plants are important components of many ecosystems and can shape community structure, it is important to understand how host-mediated interactions influence parasite preference and success. The goal of this thesis is to examine interactions between hosts, parasitic plants and herbivores mediated by chemical traits. We first examined the effects of dodder (Cuscuta sp.) parasitism on induced defenses in cranberry, and asked how cranberry chemistry affected dodder preference and performance. We found dodder preference for some cultivars, and dodder parasitism induced many changes in cranberry chemistry, which could influence other interactions with cranberry hosts. We next examined the effects of gypsy moth herbivory on cranberry chemistry, and how plant-mediated changes affected subsequent dodder preference. Herbivory delayed and reduced the number of dodder plants that attached to cranberry hosts. Herbivory also induced changes in cranberry phenolic acids and phytohormones, which could mediate defenses against dodder parasitism. We also assessed the effects of previous herbivory (by tobacco hornworm or mechanical) and previous dodder parasitism on subsequent dodder preference on tomato hosts. Previous attachment followed by removal of dodder slowed subsequent dodder attachment on tomato hosts, but prior herbivory did not affect subsequent dodder attachment. Lastly, we asked whether damage to host induced changes in the host, and if attached parasites assimilated host defenses in response to host damage. Damage to host plants induces higher jasmonic acid in both hosts and attached parasites, and herbivores fed on leaves from parasites attached to damaged hosts ate more than herbivores fed on leaves attached to undamaged parasites. In summary, these studies demonstrate that parasites can induce changes in host responses that can potentially shape other interactions with the same hosts. Similarly, both herbivores and host responses can influence parasite preference, which could alter behavior of herbivores and pollinators, shaping community dynamics.

Introduction. Primary hypobetalipoproteinemia (pHBL) is a monogenic heterogeneous condition characterized by total cholesterol (TC) and/or LDL cholesterol (LDL-C) levels below the 5th percentile of the reference population. Heterozygous APOB gene mutations are responsible for the majority of the dominant pHBL causing the familial hypobetalipoproteinemia (FHBL). The clinical phenotype of heterozygous FHBL is usually mild. The homozygous or compound heterozygous APOB mutations are in some cases responsible for a more severe biochemical and clinical phenotype, similar to the abetalipoproteinemia (ABL) due to homozygous mutations in the MTP gene, characterized by intestinal malabsorption, pigmentary retinal degeneration, ataxic neuropathy, and almost undetectable levels of LDL-C and APOB. methods and Results. In this report we describe the clinical and molecular characterization of a child with severe hypolipidemia and a clinical phenotype suggesting the clinical diagnosis of ABL. Parents serum total cholesterol (TC) and LDL cholesterol (LDLC) levels however were below the 5th percentile thus suggesting that the proband could have been homozygous or compound heterozygous FHBL. Western blot analysis showed the presence of two truncated forms of apoB protein of different molecular weight in the serum of the proband; a single truncated form was then observed in the mother on in the father. The direct sequence the apoB gene in the proband allowed to identify two novel mutations: a) a mutation of the donor splice site of intron 23 of the APOB gene (c.3824+1G>C) and b) a mutation of the acceptor site of intron 23 of of the ApoB gene (c.3825-1G>A). The parents were heterozygous carriers. Splicing mechanisms of both mutations were further characterized by minigene assay in vitro. Conclusion. In this report we have characterized at the clinical and molecular level a rare case of compound heterozygous FHBL which carries two novel splicing mutations of the APOB gene affecting the splicing machinery.