there is no such thing as an exact duplicate.
clones use a "donor" cytoplasm from another individual with it's nucleus sucked out, and the genetic material from the animal wanted to be cloned, is injected into the "nurse" cytoplasm. there is concern that methylation can be "learned" from the environment that the donor cell grew up in has information of which genes should have their expression modified, and this may in fact affect embryo development. the methylation is then signaled to inside the nucleus. methylation can be somewhat annoying.
http://www.fragilex.org/html/methylation.htm
One of the ways the cells control which genetic information they will use is to chemically modify the DNA. The illustration on the right shows an enzyme (diagrammed in ribbons) adding methyl groups to some of the DNA (balls in the form of a double helix). This inactivates that part of the chromosome. It's as if we were to put glue on the edges of some of the books in the library; those pages would become unavailable to readers.
Good methylation
In females methylation is used regularly to solve a problem. Men have only one X chromosome and women have two. As a result, female cells might be expected to make twice as much protein from the information on X chromosomes as males do. Instead, women's cells randomly pick one of the X chromosomes and turn it off by methylation. Thus both males and females have one working X chromosome in each cell and as a result, one working unit of all the genetic information on the X chromosome.
Bad methylation
As noted above, methylation is generally a useful method for turning off chromosomal information. However, in fragile X syndrome, methylation is involved in causing the disease. Near the Fragile X Mental Retardation 1 gene (FMR1) is a regulatory site called a CpG island. In most people, the site is not methylated. As a result, the cell can use the FMR1 gene when there is a need for Fragile X Mental Retardation Protein (FMRP).
these CPG islands are everywhere, and are susceptible to methylation. basically we understand nothing about this in cattle and how environment may affect this and how it is inherited and why with inputs to the cow with what she is eating, when she is eating it, selecting for cows that grow on grass, but wanting steers to gain on grain. this is very complex. i feel that some people are dead ending genetics not taking this into account and are seeing some suprising results they have no idea why they are seeing them, but they know something is going on.
what would be cool is to be able to globally analyze methylation in cow families and their offsrpring exposed to different environments, most simply fattened only on grass, fattened with a typical grass to grain system, versus as shortened fattening, all from say 20 eggs each from 4 different type females. this will come sooner than you think, and will be poo pooed. what also would be interesting is to test animals that have dominant traits for the trait of interest in both homo and hetero state and follow that as well. this methylation may be fooling us in finding linkages to traits of interest. that would be a bummer. it's tough to be thorough, and underestimated.
throw in a the twist of the ultimate steer who is a carrier for multiple genetics beyond PHA and TH, ie monkey mouth and spastic pareisis, and you are starting to multiply the conundrum rather quickly. try controlling for 4 variables in your experimental design. not for the faint of heart. that's why it's important to weed them out quickly for long term progress. i guess a steer show could evolve into selecting for embryo's that have all the defects in a carrier status with pcr on the embryo, including sex, if you want steers, but if you want to eat them, you may want a heifer, but anyway, embryologists would be making a little more money and could be sponsoring steer shows with all that extra cash. ET would then be shifted to industrialization.