No abstract

We studied the effects of mountain lion (Puma concolor) predation on 2 translocated populations of bighorn sheep (Ovis canadensis) in New Mexico, USA. During 1993, 32 Rocky Mountain bighorn sheep (O. c. canadensis) were translocated to Wheeler Peak Wilderness Area in northern New Mexico, and during 1992–1993, 31 desert bighorn sheep (O. c. mexicana) were translocated to Sierra Ladron in central New Mexico. We monitored both populations from release through 2000 using fixed‐wing aircraft and ground and/or helicopter surveys. We determined cause of mortality for radiomarked individuals (n = 26) and calculated survival rates, cause‐specific mortality rates, exponential growth rates, and lamb:ewe ratios. The post‐lambing population estimates in 2000 were 180 in Wheeler Peak and 21 in Sierra Ladron. Annual adult survival was higher (P < 0.005) in the Wheeler Peak population (0.955) than in the Sierra Ladron population (0.784). Annual lamb:ewe ratios also were higher (P < 0.001) in the Wheeler Peak population (66.7 vs. 29.8). Mean annual exponential growth rate (r) in the Wheeler Peak population was 0.25 compared to −0.01 for the Sierra Ladron population. Predation by mountain lions was the primary proximate cause (75%) of 16 known‐cause mortalities of radiomarked bighorn sheep in the Sierra Ladron population, while we did not document any predation in Wheeler Peak. The annual cause‐specific mortality rates due to mountain lion predation in Sierra Ladron were 0.13 for males, 0.09 for females, and 0.11 for all adult bighorn sheep. Mountain lion predation may have limited the Sierra Ladron bighorn sheep population and could be imposing a destabilizing inverse density‐dependent mortality. Mountain lions preyed on domestic cattle in the Sierra Ladron area and throughout desert bighorn sheep habitat in New Mexico; we therefore hypothesize that cattle “subsidized” the diets of mountain lions (i.e., reduced or eliminated natural starvation). The ultimate cause of mortality for these desert bighorn sheep may be related to subsidized mountain lion populations that do not appear to decline following native ungulate population decreases. In addition, the encroachment of woody vegetation may increase the hunting success of ambush predators like mountain lions. High mountain lion predation may require mitigation for the successful restoration of bighorn sheep.

N-Alkylpurines induced in DNA by simple monofunctional alkylating agents are known to be cytotoxic and possibly indirectly mutagenic. These adducts are removed by the ubiquitous N-methylpurine-DNA glycosylase (MPG) in a multistep repair pathway. Chinese hamster ovary (CHO) cell clones expressing 2- to 16-fold enhanced levels of MPG activity were isolated from cells stably transfected with human MPG cDNA expression plasmids. The in vivo removal of 3-methyladenine and 7-methylguanine from some of these lines was analyzed and was observed to reflect their MPG levels. These cell lines did not develop increased resistance, as compared to the control, in regards to cytotoxic, mutagenic and sister chromatid exchange inducing effects of the alkylating agents that induce 3-alkyladenine and 7-alkylguanine as the major alkyl adducts in DNA. These results suggest that the MPG activity is not limiting in the multi-step repair pathway of N-alkylpurines in CHO cells.

chromosomes resemble each other closely within synOne of the larger contiguous blocks of mouse-hu-tenic blocks that vary widely in size, containing just man genomic homology includes the proximal portion a few to several hundred related genes (reviewed by of mouse chromosome 7 and the long arm of human Copeland et al., 1993). Within the best-mapped of these chromosome 19. Previous studies have demonstrated syntenically homologous regions, the presence and lothe close relationship between the two regions, but cation of specific genes can be accurately predicted in have also indicated significant rearrangements in the one species, based upon the mapping results obtained relative orders of homologous mouse and human in the other. In many cases, information regarding gene genes. Here we present the genetic locations of the function derived from the analysis of human hereditary homologs of 42 human chromosome 19q markers in the traits or mapped murine mutations may also be extrapmouse, with an emphasis on genes also included in olated from one species to another (e.g., Ton et al., 1992; the human chromosome 19 physical map. Our results Giebel and Spritz, 1991). However, local rearrangedemonstrate that despite an overall inversion of sements, including apparent deletions, inversions, inserquences relative to the centromere, apparent ''transtions, and transposition events, have occurred within positions'' of three gene-rich segments, and a local inthese homologous blocks during the course of evolution, version of markers mapping near the 19q telomere, gene content, order, and spacing are remarkably well so that relationships between syntenically homologous conserved throughout the lengths of these related mouse and human regions are not always as straightmouse and human regions. Although most human 19q forward as they may seem on the grosser level. Consemarkers have remained genetically linked in mouse, quently, the power of prediction afforded in any homolone small human segment forms a separate region of ogy region increases tremendously with the level of reshomology between human chromosome 19q and mouse olution and degree of internal consistency associated chromosome 17. Three of the four rearrangements of with a particular set of comparative mapping data. mouse versus human 19q sequences involve segmentsOne of the larger contiguous blocks of mouse-human that are located directly adjacent to each other in genomic homology includes the proximal portion of portant new tool to aid in the mapping of genes and Cavanna et al., 1990; Brown et al., 1993; reviewed by associated phenotypes in both species. ᭧ 1996 Academic Press, Inc. Brilliant et al., 1994), but have also indicated that a significant amount of rearrangement has occurred between the mouse and the human segments. The recent

Chinese hamster ovary cells with no detectable (less than 200 molecules/cell) O6-methylguanine-DNA methyltransferase (EC 2.1.1.63) were transfected with human cell DNA and pSV2neo plasmid by electroporation. Two stable transformant clones, GC-1 and GC-2, containing 4 X 10(4) and 4-6 X 10(3) methyltransferase molecules/cell respectively were isolated by successive screening in the presence of G418 and 2-chloroethyl-N-nitrosourea (CNU). Only three or four copies of pSV2neo DNA and no repetitive human DNA sequence were detected in these isolates. Secondary transfection of parent cells with GC-1 DNA yielded several clones containing 2-10 X 10(3) methyltransferase molecules/cell. The rate of removal of O6-methylguanine in GC-1, GC-2 and parent cells in vivo reflected their methyltransferase levels, while the N-methylpurines were removed at similar rates in all three cell lines. The differential sensitivity of these cells to several alkylating agents, namely CNU, N-methyl-N-nitrosourea, N-methyl-N'-nitro-N-nitrosoguanidine and methyl-methane sulfonate (MMS), known to yield different proportions of O6-alkylguanine among the alkyl adducts in DNA, varied widely. The largest and smallest differences in toxic response were observed with CNU and MMS respectively. These cell lines showed no difference in sensitivity to the DNA cross-linking agent psoralen. These data strongly suggest that alkylating agents produce two classes of lethal lesions, one of which is O6-alkylguanine. Induction of mutations at the hypoxanthine-phosphoribosyltransferase locus in these cells lines suggests that, regardless of its relative yield, O6-methylguanine is the major mutagenic lesion for all alkylating agents.