Submitted to: Society for the Study of Reproduction Annual Meeting
Publication Type: Abstract Only
Publication Acceptance Date: May 1, 2004
Publication Date: July 1, 2004
Citation: Guthrie, H.D., Wall, R.J., Pursel, V.G., Foster Frey, J.A., Donovan, D.M., Welch, G.R., Garrett, W.M. 2004. Follicular expression of a human beta-cell leukemia/lymphoma-2 (bcl-2)transgene does not decrease atresia or increase ovulation rate in swine. Society for the Study of Reproduction Annual Meeting. Abstract. p275.
Transgenic gilts carrying a mouse inhibin alpha subunit promoter driving a human Bcl-2 cDNA transgene were used to determine if ectopic expression of Bcl-2 in the ovaries would decrease the frequency of atresia in antral follicles and increase ovulation rate. Three transgenic lines consisting of 151 pigs were generated by pronuclear injection and embryo transfer. Bcl-2 was ectopically expressed in the ovary, Leydig cells, and adrenal cortex in lines 1 and 3, but not in line 2. Immunohistochemical analysis showed that in transgenic gilts, Bcl-2 was expressed in granulosa (GC) and theca (TC) cells in a greater proportion (P < 0.01) of healthy than atretic follicles. In prepubertal gilts (n = 12, lines 1 and 3 combined) Bcl-2 expression in healthy and atretic follicles was 61 vs. 23% for GC and 67 vs. 33% for TC, respectively. In day 50 pregnant (line 1) gilts (n = 12) Bcl-2 expression in healthy and atretic follicles was 96 vs. 66% for GC and 89 vs. 57% for TC, respectively. In contrast, Bcl-2 protein was expressed in only 1.4% of healthy and 0% of atretic follicles in prepubertal and day 50 pregnant nontransgenic littermates (n = 13). Despite ectopic expression of Bcl-2 in most healthy and many atretic follicles, the atresia rate did not differ (P > 0.05) between transgenic and nontransgenic littermates; prepubertal (45 vs. 59%) and day 50 pregnant (53 vs. 52%), respectively. The mean ovulation rate did not differ (P > 0.05) between transgenic (n = 12) and nontransgenic (n = 7) day 50 pregnant gilts, 15.9 and 16.4, respectively. The molecular basis of the failure of ectopic Bcl-2 expression to increase the ratio of healthy to atretic follicles is unknown, but it is possible that the activity of the mitochondrial-dependent cell death pathway was not neutralized by ectopic expression of human Bcl-2 or that other cell death pathways compensated for the decreased mitochondrial-dependent cell death.