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The evolution of the major histocomp...

Hess, Christopher M.

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The evolution of the major histocompatibility complex in house finches (Carpodacus mexicanus).

Record Type:	Language materials, printed : Monograph/item
Title/Author:	The evolution of the major histocompatibility complex in house finches (Carpodacus mexicanus)./
Author:	Hess, Christopher M.
Description:	96 p.
Notes:	Chair: Sievert A. Rohwer.
Contained By:	Dissertation Abstracts International66-06B.
Subject:	Biology, Ecology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3178145
ISBN:	9780542177200

The evolution of the major histocompatibility complex in house finches (Carpodacus mexicanus).
Hess, Christopher M.

The evolution of the major histocompatibility complex in house finches (Carpodacus mexicanus). - 96 p.

Chair: Sievert A. Rohwer.

Thesis (Ph.D.)--University of Washington, 2005.

Understanding the mechanisms shaping the genetic variation in populations is one of the central questions in evolutionary biology. I have explored the effects of natural selection on a population of house finches (Carpodacus mexicanus) for disease resistance in response to a novel bacterial pathogen, Mycoplasma gallisepticum. Over the last fifteen years infection by Mycoplasma has caused a dramatic decline in population number in the eastern United States. During this time, researchers have also observed marked decreases in observable levels of pathogenesis, most likely caused by an increase in levels of resistance. I utilized large scale sequencing techniques to examine genes from the major histocompatibility complex (MHC) to explore their role as candidate genes for resistance and explore the benefits of this approach in a review on the mechanisms of MHC evolution in birds, which differ markedly from the patterns that have become ubiquitous for the mammalian MHC. My initial approach to isolate these genes via cosmid libraries yielded a non-functional pseudogene containing several frameshift mutations and stop codons in exons that make up the peptide-binding region of the MHC receptor. The levels of variability found in this pseudogene were higher than that of the background nuclear genome in house finches, probably resulting from genetic hitchhiking with genes under selection or as a signal of selection on the gene prior to loss of function. Subsequent isolation attempts with the polymerase chain reaction allowed for amplification of a functional MHC devoid of frameshift or nonsense mutations. Analysis of diachronic samples of these genes prior to exposure to Mycoplasma and more recently show shifts in allele frequencies since introduction of the pathogen, but most of these changes are also observed in control populations not exposed to the bacteria. Expression studies show decreased expression of the MHC following exposure to Mycoplasma, a result that is consistent with cytomegalovirus in mice and potentially indicates manipulation of the immune system by the pathogen. These results represent the first attempt to understand a natural experiment in the evolution of resistance to Mycoplasma in house finches.

ISBN: 9780542177200Subjects--Topical Terms:

1017726
Biology, Ecology.

The evolution of the major histocompatibility complex in house finches (Carpodacus mexicanus).
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100 1 $a Hess, Christopher M. $3 1281911
245 1 4 $a The evolution of the major histocompatibility complex in house finches (Carpodacus mexicanus).
300 $a 96 p.
500 $a Chair: Sievert A. Rohwer.
500 $a Source: Dissertation Abstracts International, Volume: 66-06, Section: B, page: 3001.
502 $a Thesis (Ph.D.)--University of Washington, 2005.
520 $a Understanding the mechanisms shaping the genetic variation in populations is one of the central questions in evolutionary biology. I have explored the effects of natural selection on a population of house finches (Carpodacus mexicanus) for disease resistance in response to a novel bacterial pathogen, Mycoplasma gallisepticum. Over the last fifteen years infection by Mycoplasma has caused a dramatic decline in population number in the eastern United States. During this time, researchers have also observed marked decreases in observable levels of pathogenesis, most likely caused by an increase in levels of resistance. I utilized large scale sequencing techniques to examine genes from the major histocompatibility complex (MHC) to explore their role as candidate genes for resistance and explore the benefits of this approach in a review on the mechanisms of MHC evolution in birds, which differ markedly from the patterns that have become ubiquitous for the mammalian MHC. My initial approach to isolate these genes via cosmid libraries yielded a non-functional pseudogene containing several frameshift mutations and stop codons in exons that make up the peptide-binding region of the MHC receptor. The levels of variability found in this pseudogene were higher than that of the background nuclear genome in house finches, probably resulting from genetic hitchhiking with genes under selection or as a signal of selection on the gene prior to loss of function. Subsequent isolation attempts with the polymerase chain reaction allowed for amplification of a functional MHC devoid of frameshift or nonsense mutations. Analysis of diachronic samples of these genes prior to exposure to Mycoplasma and more recently show shifts in allele frequencies since introduction of the pathogen, but most of these changes are also observed in control populations not exposed to the bacteria. Expression studies show decreased expression of the MHC following exposure to Mycoplasma, a result that is consistent with cytomegalovirus in mice and potentially indicates manipulation of the immune system by the pathogen. These results represent the first attempt to understand a natural experiment in the evolution of resistance to Mycoplasma in house finches.
590 $a School code: 0250.
650 4 $a Biology, Ecology. $3 1017726
650 4 $a Biology, Genetics. $3 1017730
650 4 $a Biology, Zoology. $3 1018632
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