redfornow":1sbcljyw said:
HerefordSire":1sbcljyw said:
these are probability numbers, not actual returns on percentage of desirable alleles, elimination of undesirables, and doesn't even take into account accumulated environmental response stored in methylation.
Nice input!
I encourage you to post all ye know on the subject so we can learn.
They did! It was almost 2 full lines long....
Actually, knabe was just pointing out that the tradional way that most cattleman refer to pedigrees and the "blood percentage" of ancestors in it is a misnomer. While the probability is good that an animal contains "genes" approximately equivalent to that percentage tracing back to the ancestor, within a couple of standard deviations (especially if close up), the THEORETICAL possiblity actually can range from 0% up to 50% on any ancestors who are not the parents. If an ancestor appears in the pedigree of BOTH parents then the theoretical range of possibility increases to from 0% up to 100%. So, theoretically, by linebreeding cattle with a common ancestor top and bottom, a breeder could end up with a descendant that carries close to 100% of the genes of the common ancestor. One would hope that by selecting for the outstanding traits of a common ancestor and culling against undesirable traits, the next generations will be better than the ancestor.
Outliers can certainly occur and they are often the best or the worst individuals, when judged phenotypically or performance wise. One purpose of linebreeding is to increase the homozygousity of genes in a line of cattle and improve the predictability of what will be produced going forward. Use of an outstanding outlier in a linebreeding program can actually reduce predictability for a generation or two.
My goal, in breeding my herd sire back to a dozen of his daughters, was an effort to make sure there wasn't any simple recessive genes lurking that would cause significant harm in a linebreeding program. A genetic gutcheck before getting too deep into the breeding program. The results should also accentuate the strong points and the faults, making them more evident.
The dwarfism gene that devastated Hereford herds in the 40s and 50s and, most recently, the IE gene are two examples of simple recessive genes.
Luckily, the bovine genome has been mapped and the "offending gene" that causes IE has been identified, including its source where the mutation occurred, and a test was developed so a breeder can just test for its presence.
Such tests weren't available in the 40s and 50s. In the days of dwarfism, the way breeders "proved" that their Hereford herd sires were dwarfism free was to mate them to a dozen or so of their daughters. If a dwarf calf didn't occur in those matings, then the probablity that the herd sire had the dwarfism gene was reduced to virtually zero. The Prospector line of Herefords that later became the foundation of Frank Felton's program was a line that was bred from Hereford cattle containing the dwarf gene. They were linebred to prove that you could successfully breed the dwarfism gene out, by testing for its presence via linebreeding.
The methylation mentioned in knabe's post interests me. I'm interested in knowing how that might affect phenotype and performance variations in closely related individuals.
George