Inheritance of fertility in broiler chickens

Background

The fertility of a chicken''s egg is a trait which depends on both the hen that lays the egg and on her mate. It is also known that fertility of an individual changes over the laying period.

Methods

Longitudinal models including both random genetic and permanent environmental effects of both the female and her male mate were used to model the proportion of fertile eggs in a pedigree broiler population over the ages 29-54 weeks.

Results

Both the male and the female contribute to variation in fertility. Estimates of heritability of weekly records were typically 7% for female and 10% for male contributions to fertility. Repeatability estimates ranged from 24 to 33%, respectively. The estimated genetic variance remained almost constant for both sexes over the laying period and the genetic correlations between different ages were close to 1.0. The permanent environment components increased substantially towards the end of the analyzed period, and correlations between permanent environment effects at different ages declined with increasing age difference The heritability of mean fertility over the whole laying period was estimated at 13% for females and 17% for males. A small positive correlation between genetic effects for male and female fertility was found.

Conclusion

Opportunities to improve fertility in broiler stocks by selection on both sexes exist and should have an impact throughout the laying period.     

Genetic heterogeneity of residual variance in broiler chickens

Aims were to estimate the extent of genetic heterogeneity in environmental variance. Data comprised 99 535 records of 35-day body weights from broiler chickens reared in a controlled environment. Residual variance within dam families was estimated using ASREML, after fitting fixed effects such as genetic groups and hatches, for each of 377 genetically contemporary sires with a large number of progeny (> 100 males or females each). Residual variance was computed separately for male and female offspring, and after correction for sampling, strong evidence for heterogeneity was found, the standard deviation between sires in within variance amounting to 15–18% of its mean. Reanalysis using log-transformed data gave similar results, and elimination of 2–3% of outlier data reduced the heterogeneity but it was still over 10%. The correlation between estimates for males and females was low, however. The correlation between sire effects on progeny mean and residual variance for body weight was small and negative (-0.1). Using a data set bigger than any yet presented and on a trait measurable in both sexes, this study has shown evidence for heterogeneity in the residual variance, which could not be explained by segregation of major genes unless very few determined the trait.     

Aflatoxicosis in rabbits: Effectiveness of Egyptian raw bentonite in prevention or diminution the detrimental effects of naturally aflatoxin contaminated diets

Thirty five females and 15 males of New Zealand White mature rabbits about 6 months of age, were assigned to 1–5 dietary treatments (7 does+3 bucks for each): uncontaminated control diet, naturally aflatoxin contaminated diet without or with 1,2 and 3% bentonite. Rabbit fed with the aflatoxin-diet had a decreased (P<0.01 or 0.05) physical semen characteristics of bucks and a reproductive performance traits of does. The values of conception rate (%), gestation length (days), litter size (n) and litter weights (g) at birth and viability (%) of litters of doe rabbits, fed with the aflatoxin-diet, recorded, respectively: 64.5; 31.0; 4.4; 275.0 and 57.1 versus 85.6; 30.3; 7.9; 508.0; and 100 for those fed with the uncontaminated diet. Addition of bentonite to the aflatoxin contaminated diet improved in general the physical semen characteristics of buck and reproductive performance traits of doe rabbits. The results of the study demonstrate that adding 1% of Egyptian raw bentonite to the naturally aflatoxin contaminated rabbit diets can provide an effective, cheap and safe practical technique for preventing the aflatoxicosis in mature rabbits.     

Cytoplasmic filaments and cellular wound healing in amoeba proteus

The flexibility and self-healing properties of animal cell surface membranes are well known. These properties have been best exploited in various micrurgical studies on living cells (2, 3), especially in amoebae (7, 20). During nuclear transplantation in amoebae, the hole in the membrane through which a nucleus passes can have a diameter of 20-30 μm, and yet such holes are quickly sealed, although some cytoplasm usually escapes during the transfer. While enucleating amoebae in previous studies, we found that if a very small portion of a nucleus was pushed through the membrane and exposed to the external medium, the amoeba expelled such a nucleus on its own accord. When this happened, a new membrane appeared to form around the embedded portion of the nucleus and no visible loss of cytoplasm occurred during nuclear extrusion. In the present study, we examined amoebae that were at different stages of expelling partially exposed nuclei, to follow the sequence of events during the apparent new membrane formation. Unexpectedly, we found that a new membrane is not formed around the nucleus from inside but a hole is sealed primarily by a constriction of the existing membrane, and that cytoplasmic filaments are responsible for the prevention of the loss of cytoplasm.     

Identification of Mixed Lineage Leukemia 1(MLL1) Protein as a Coactivator of Heat Shock Factor 1(HSF1) Protein in Response to Heat Shock Protein 90 (HSP90) Inhibition

Heat shock protein 90 (HSP90) inhibition inhibits cancer cell proliferation through depleting client oncoproteins and shutting down multiple oncogenic pathways. Therefore, it is an attractive strategy for targeting human cancers. Several HSP90 inhibitors, including AUY922 and STA9090, show promising effects in clinical trials. However, the efficacy of HSP90 inhibitors may be limited by heat shock factor 1 (HSF1)-mediated feedback mechanisms. Here, we identify, through an siRNA screen, that the histone H3 lysine 4 methyltransferase MLL1 functions as a coactivator of HSF1 in response to HSP90 inhibition. MLL1 is recruited to the promoters of HSF1 target genes and regulates their expression in response to HSP90 inhibition. In addition, a striking combination effect is observed when MLL1 depletion is combined with HSP90 inhibition in various human cancer cell lines and tumor models. Thus, targeting MLL1 may block a HSF1-mediated feedback mechanism induced by HSP90 inhibition and provide a new avenue to enhance HSP90 inhibitor activity in human cancers.