Concerns over declining mule deer (Odocoileus hemionus) populations during the 1990s prompted research efforts to identify and understand key limiting factors of deer. Similar to past deer declines, a top priority of state wildlife agencies was to evaluate the relative importance of habitat and predation. We therefore evaluated the effect of enhanced nutrition of deer during winter and spring on fecundity and survival rates using a life table response experiment involving free‐ranging mule deer on the Uncompahgre Plateau in southwest Colorado, USA. The treatment represented an instantaneous increase in nutritional carrying capacity of a pinyon (Pinus edulis)—Utah juniper (Juniperus osteosperma) winter range and was intended to simulate optimum habitat quality. Prior studies on the Uncompahgre Plateau indicated predation and disease were the most common proximate causes of deer mortality. By manipulating nutrition and leaving natural predation unaltered, we determined whether habitat quality was ultimately a critical factor limiting the deer population. We measured annual survival and fecundity of adult females and survival of fawns, then estimated population rate of change as a function of enhanced nutrition. Pregnancy and fetal rates of adult females were high and did not vary in response to treatment. Fetal and neonatal survival rates increased in response to treatment, although the treatment effect on neonatal survival was marginal. Overwinter rates of fawn survival increased for treatment deer by 0.16–0.31 depending on year and fawn sex, and none of the 95% confidence intervals associated with the effects overlapped zero. Overwinter rates of fawn survival averaged 0.905 (SE = 0.026) for treatment deer and 0.684 (SE = 0.044) for control deer. Nutritional enhancement increased survival rates of fetuses to the yearling age class by 0.14–0.20 depending on year and fawn sex; 95% confidence intervals slightly overlapped zero. When averaging estimates across sexes and years, treatment caused fetal to yearling survival to increase by 0.177 (SE = 0.082, 95% CI: 0.016–0.337). Annual survival of adult females receiving treatment (Ś = 0.879, SE = 0.021) was higher than survival of control adult females (Ś = 0.833, SE = 0.025). Our estimate of the population rate of change (λ) was 1.165 (SE = 0.036) for treatment deer and 1.033 (SE = 0.038) for control deer. Increased production and survival of young (i.e., fetal, neonatal, and overwinter fawn survival) accounted for 64% of the overall increase in λ, whereas adult female survival accounted for 36% of the increase in λ. The effect of nutrition treatment on overwinter fawn survival alone accounted for 33% of the overall increase in λ. We documented food limitation in the Uncompahgre deer population because survival of fawns and adult females increased considerably in response to enhanced nutrition. We found strong evidence that enhanced nutrition of deer reduced coyote (Canis latrans) and mountain lion (Puma concolor) predation rates of ≥6‐month‐old fawns and adult...

Estimating survival of the offspring of marked female ungulates has proven difficult in free-ranging populations yet could improve our understanding of factors that limit populations. We evaluated the feasibility and efficiency of capturing large samples (i.e., .80/yr) of neonate mule deer (Odocoileus hemionus) exclusively from free-ranging, marked adult females using vaginal implant transmitters (VITs, n ¼ 154) and repeated locations of radiocollared females without VITs. We also evaluated the effectiveness of VITs, when used in conjunction with in utero fetal counts, for obtaining direct estimates of fetal survival. During 2003 and 2004, after we placed VIT batteries on a 12-hour duty cycle to lower electronic failure rates, the proportion that shed 3 days prepartum or during parturition was 0.623 (SE ¼ 0.0456), and the proportion of VITs shed only during parturition was 0.447 (SE ¼ 0.0468). Our neonate capture success rate was 0.880 (SE ¼ 0.0359) from females with VITs shed 3 days prepartum or during parturition and 0.307 (SE ¼ 0.0235) from radiocollared females without VITs or whose implant failed to function properly. Using a combination of techniques, we captured 275 neonates and found 21 stillborns during 2002À2004. We accounted for all fetuses at birth (i.e., live or stillborn) from 78 of the 147 females (0.531, SE ¼ 0.0413) having winter fetal counts, and this rate was heavily dependent on VIT retention success. Deer that shed VITs prepartum were larger than deer that retained VITs to parturition, indicating a need to develop variable-sized VITs that may be fitted individually to deer in the field. We demonstrated that direct estimates of fetal and neonatal survival may be obtained from previously marked female mule deer in free-ranging populations, thus expanding opportunities for conducting field experiments. Survival estimates using VITs lacked bias that is typically associated with other neonate capture techniques. However, current vaginal implant failure rates and overall expense limit broad applicability of the technique. (JOURNAL OF WILDLIFE MANAGEMENT 71(3): 945-954; 2007)

We have identified the disulfide cross-links in bull protamine by titrating intact bull sperm with dithiothreitol (DTT) and following the modification of each cysteine residue with tritiated iodoacetate. The derivatization of each cysteine was monitored by a combination of HPLC, peptide mapping, and protein sequencing. Analyses of total free sulfhydryls show that all seven of the bull protamine cysteines are cross-linked as disulfides in mature sperm. The first disulfide is reduced at a DTT:protamine cysteine (DTT:Cys) ratio of 0.3 and the last at a ratio of 2.0. Intra- and intermolecular disulfides were identified by correlating the reduction of specific disulfides with the dissociation of protamine from DNA in partially reduced sperm and sperm treated with N,N'-ethylenedimaleimide, a bifunctional disulfide cross-linking agent. Three intermolecular and two intramolecular disulfides were identified. The results of these experiments demonstrate that the amino- and carboxy-terminal ends of the bull protamine molecule are folded inward toward the center of the molecule and are locked in place, each by a single intramolecular disulfide bridge. Three intermolecular disulfides cross-link neighboring protamine molecules around the DNA helix in such a manner that the protamines cannot be dissociated from DNA without first reducing the interprotamine disulfides.

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