Hominoid primate species differ remarkably in their social grouping and mating systems, notably including differing degrees of post-copulatory sexual selection. As the mating system of extinct hominins remains unknown and difficult to predict, it may be useful to examine more proximate phenotypes correlated with behavior. For example, chimpanzees and bonobos have a large ejaculate that coagulates into a rigid copulatory plug, presumably in response to high levels of sperm competition, while gorillas have a small semi-viscous ejaculate associated with low sperm competition. To understand the molecular basis responsible for differences in semen biochemistry among hominoid species, I completed two research projects. First, by cloning the upstream putative promoters of the chimpanzee, bonobo, human, and gorilla prostatic acid phosphatase (ACPP) genes into luciferase reporter vectors followed by transient transfections into a human prostate cell line, I identified the underlying nucleotide changes that reduce expression of this protein in chimpanzee semen. Second, by mapping large deletions at the kallikrein-related peptidase (KLK) locus in the gorilla and gibbon genomes, I characterized the convergent gene loss and the formation of a novel chimeric gene in these monandrous species. For both the ACPP and KLK locus changes, I determined the polarity of the changes through outgroup comparison. At ACPP, the reduced expression in chimpanzee and bonobo is derived, and likely in response to the onset of intense sperm competition in the common ancestor of these two species. If this biochemical phenotype is indeed a proxy for mating behavior, my data provides some evidence (to be compared and contrasted with other molecular, behavioral, and paleontological data) that the last common ancestor of humans and chimpanzees was not chimp-like in its high degree of polyandry. / Bayer School of Natural and Environmental Sciences; / Biological Sciences / PhD; / Dissertation;

Prostate cancer is one of the most common malignant tumors in solid organs of old men. However, the patients are nearly 100 percent survivable if detected early. Prostate-specific antigen (PSA) is a valuable prostate cancer biomarker that is now wildly used for population screening, diagnosis, and monitoring of patients with prostate cancer. But PSA is not good enough for a biomarker because it can not distinguish benign prostate hyperplasia (BPH) from prostate tumor . Recently, there are some tumor marker still in study, for example: free prostate specific antigen¡]fPSA), complexed prostate specific antigen (C-PSA), kallikrein,prostate specific membrane antigen (PSMA). From previously study,we had found many different protein expressions between serum of normal and prostate patients. Mayven is one of the novel proteins that had been identified. The mRNA expression of Mayven in prostate cancer tissue is determined by quantitative RT-PCR. The result shows that the mRNA expression of Mayven in Benign Prostatic Hyperplasia (BPH) is about 5.0-11.3 fold than normal tissue , 12.7 fold in Prostate Cancer (PCa) stage T1 and 0.1- 3.7 fold after cancer stage T2. The Mayven gene expression is predominate in tumor stage T1, decrease after T2 stage. However the expressed pattern of mayven in BPH remains further investigation due to the limited sample size. Furthermore, with 2 dimensional electrophoresis (2¡VDE), we have found 7 differentially expressed proteins between tissue of normal and prostate patients, and these proteins are identified by MALDI-TOF mass spectrometry and MS-Fit. These identified proteins are Keratin 8¡]KRT8¡^, MAPKkinase5¡]MAP2K5¡^, Acid phosphatase (ACPP), Annexin A3¡]ANXA3¡^, Phosphoglycerate mutase 1 (PGAM1), Spindlin-like protein 2 (SPIN2) and Transgelin 2¡]TAGLN2¡^.