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   <dim:field mdschema="dc" element="contributor" qualifier="advisor">Kim, Dennis H.</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="author">Boor, Sonia</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="department">Massachusetts Institute of Technology. Department of Biology</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="accessioned">2023-01-19T19:49:28Z</dim:field>
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   <dim:field mdschema="dc" element="date" qualifier="issued">2022-09</dim:field>
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   <dim:field mdschema="dc" element="description" qualifier="abstract">The ability to adapt to changes in food conditions is critical for organismal homeostasis and survival. In this thesis, I explore the genetic and neuroendocrine mechanisms by which C. elegans evaluates bacterial food conditions and accordingly alters development and behavior. In Chapter One, I discuss the relationship between C. elegans and its bacterial diet. The influence of food on behavior suggests the presence of a gut-“brain” axis that senses and communicates information about nutritional state to the nervous system to elicit a behavioral response.&#xd;
&#xd;
In Chapter Two, I characterize a gain-of-function allele of scd-2, the C. elegans Anaplastic Lymphoma Kinase (ALK) gene ortholog, scd-2(syb2455),which I designed based on an oncogenic mutation in ALK. While animals with loss-of-function mutations in scd-2 are dauer-formation defective, scd-2(syb2455) animals enter dauer regardless of food conditions. In Chapter Three, I report that SCD-2 also regulates the food-dependent feeding and foraging behaviors known as dwelling and roaming; scd-2(syb2455) animals roam more and scd-2 loss-of-function animals roam less than wild type. Additionally, in contrast to wild-type animals, which express the gene encoding the TGF- signaling ligand DAF-7 exclusively in the ASI chemosensory neurons, scd-2(syb2455) animals constitutively express daf-7 in both the ASI and ASJ neurons. The expression of daf-7 in the ASJ neurons drives roaming in these animals. I demonstrate that daf-7 expression in the ASJ neurons is also affected by food; ingested food in the pharynx inhibits daf-7 expression in the ASJ neurons through SCD-2 signaling. From these data we propose a positive-feedback loop that regulates roaming behavior: in the absence of ingested food, active SCD-2 induces daf-7 expression in the ASJ neurons to promote roaming, which further reduces food consumption. To further investigate how daf-7 neuroendocrine signaling responds to nutritional state, in Chapter Four I describe a screen for satiety signals using the nutritional state-dependent daf-7 expression in the ASJ neurons in males as a readout for communication along the gut-“brain” axis. This screen yielded a loss-of-function allele of che-3 and a gain-of-function allele of pdfr-1. In Chapter Five, I discuss future directions for investigating how C. elegans interacts with its food environment.</dim:field>
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   <dim:field mdschema="dc" element="title">Genetic Analysis of Bacterial Food Perception and its Influence on Foraging Behavior in C. elegans</dim:field>
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   	&lt;Title>Genetic Analysis of Bacterial Food Perception and its Influence on Foraging Behavior in C. elegans&lt;/Title>
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   	&lt;Abstract>The ability to adapt to changes in food conditions is critical for organismal homeostasis and survival. In this thesis, I explore the genetic and neuroendocrine mechanisms by which C. elegans evaluates bacterial food conditions and accordingly alters development and behavior. In Chapter One, I discuss the relationship between C. elegans and its bacterial diet. The influence of food on behavior suggests the presence of a gut-“brain” axis that senses and communicates information about nutritional state to the nervous system to elicit a behavioral response.&#xd;
&#xd;
In Chapter Two, I characterize a gain-of-function allele of scd-2, the C. elegans Anaplastic Lymphoma Kinase (ALK) gene ortholog, scd-2(syb2455),which I designed based on an oncogenic mutation in ALK. While animals with loss-of-function mutations in scd-2 are dauer-formation defective, scd-2(syb2455) animals enter dauer regardless of food conditions. In Chapter Three, I report that SCD-2 also regulates the food-dependent feeding and foraging behaviors known as dwelling and roaming; scd-2(syb2455) animals roam more and scd-2 loss-of-function animals roam less than wild type. Additionally, in contrast to wild-type animals, which express the gene encoding the TGF- signaling ligand DAF-7 exclusively in the ASI chemosensory neurons, scd-2(syb2455) animals constitutively express daf-7 in both the ASI and ASJ neurons. The expression of daf-7 in the ASJ neurons drives roaming in these animals. I demonstrate that daf-7 expression in the ASJ neurons is also affected by food; ingested food in the pharynx inhibits daf-7 expression in the ASJ neurons through SCD-2 signaling. From these data we propose a positive-feedback loop that regulates roaming behavior: in the absence of ingested food, active SCD-2 induces daf-7 expression in the ASJ neurons to promote roaming, which further reduces food consumption. To further investigate how daf-7 neuroendocrine signaling responds to nutritional state, in Chapter Four I describe a screen for satiety signals using the nutritional state-dependent daf-7 expression in the ASJ neurons in males as a readout for communication along the gut-“brain” axis. This screen yielded a loss-of-function allele of che-3 and a gain-of-function allele of pdfr-1. In Chapter Five, I discuss future directions for investigating how C. elegans interacts with its food environment.&lt;/Abstract>
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