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To: RightWingNilla
Scientists routinely take genes out and put foreign genes into mice. For many of the changes, the animals don't cease to develop but instead show a different phenotype than the wild type mouse.

Experiments of inserting foreign genes into yeasts have been successful but yeasts do not have much non-coding DNA to bother with. The insertion of foreign genetic material into mice though is quite complicated:

Using recombinant DNA methods, build molecules of DNA containing
* the structural gene you desire (e.g., the insulin gene)
* vector DNA to enable the molecules to be inserted into host DNA molecules
* promoter and enhancer sequences to enable the gene to be expressed by host cells
From: Transgenic Animals

Not so easy and note that they have to take not just the gene, but other sequences from the genome in order to make it usable.

With current protocols for the creation of transgenic mice by embryo microinjection, the site of integration is not predetermined, and, for all practical purposes, should be considered random. Microinjection allows one to add, but not subtract genetic material in a directed manner; if a particular experiment leads to the insertion of an novel version of a mouse gene into the genome, this novel allele will be present in addition to the normal diploid pair. Consequently, only dominant, or co-dominant, forms of phenotypic expression will be detectable from the transgene....

... recessive phenotypes are most likely due to the disruption of some normal vital gene. In less frequent cases, a transgene may land at a site that is flanked by an endogenous enhancer which can stimulate gene activity at inappropriate stages or tissues. This can lead to the expression of dominant phenotypes that are not strictly a result of the transgene itself. 39 For all of these reasons, it is critical to analyze data from three or more founder lines with the same transgene construct before reaching conclusions concerning the effect, or lack thereof, on the mouse phenotype....

Unless a particular transgenic insertion causes an easily detectable, dominant phenotype, the presence of the transgene in an animal is most readily determined through DNA analysis....

In the vast majority of cases, however, homozygous Tg/Tg animals will be indistinguishable in phenotype from heterozygous Tg/+ animals, and without a recessive phenotype, the identification of homozygous animals will not be straightforward.
From:   Transgenic Mouse

Note that the above shows the insertion of an additional gene. Note that the random insertion can cause death if is ends up in a vital part of the genome. Note that the inserted gene must be a dominant one. Note that even if all the above happens though - that it is hard to figure out if the gene is present in subsequent generations because most likely being an additional gene it does not get used! They have to basically search the genome to see if the gene was passed on!

1,362 posted on 06/19/2002 8:32:06 PM PDT by gore3000
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To: gore3000
Using recombinant DNA methods, build molecules of DNA containing
* the structural gene you desire (e.g., the insulin gene)
* vector DNA to enable the molecules to be inserted into host DNA molecules
* promoter and enhancer sequences to enable the gene to be expressed by host cells
From: Transgenic Animals

Not so easy and note that they have to take not just the gene, but other sequences from the genome in order to make it usable.
NO - As RightWingNilla tried to explain to you yesterday in post 1107, the promoter & enhancer regions are considered to be part of the gene.
Typically when you refer to a gene you are talking about not just the protein coding regions, but also the elements upstream which regulate its expression. Also introns break-up the protein coding region and may themselves regulate transcription. The stop codon is not where it ends though either, you have regions further transcribed downstream which will contain information which regulates how stable the mRNA is and how efficiently it will be translated. None of this is new to anyone and it is generally not what we are talking about when we are talking about Junk DNA. There are vast stretches of DNA in the genome which are nowhere near a gene or ceratinly not close enough to have any effect on gene expression via the mechanisms we know of. Perhaps there are indirect effects....?

The "junk DNA" consists of the 95% of the genome after allowing for the exons, introns, promoters, and other regulatory parts.

As RightWingNilla says, maybe, just maybe there is some regulatory effects from the 95% that is apparent junk, although I suspect its role has been in regulating evolution itself by helping to separate the gene parts that got duplicated over time into functional groups, so that the protein parts that got duplicated tended to be discrete structural lengths of proteins. This had at least 2 advantages that I can think of. Maybe I'll go into it further someday. (But not tonite. The role of the junk is purely my speculation, anyway.)

1,381 posted on 06/19/2002 11:27:59 PM PDT by jennyp
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To: gore3000
Nice summary of how trangenics are made, but I dont see how this supports your notion that the genome can't handle change which what I was arguing with you about in the first place. I have read hundreds of papers on "knockout" and "knock-in" mice and the results vary tremednously. Sometimes if the gene disrupts a critical developmental program, they die in the embryoinc stage. Sometimes the mice live longer. Clearly the genome can handle change.
1,403 posted on 06/20/2002 8:06:42 AM PDT by RightWingNilla
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