What about those jumping genes?

So there you have it, HM.I found the DNA evidence for you.

However. I'd still like to see some proof of DNA in tsetse fly spit. ("Why not? It's in human spit." is not good enough.

I'd also like to see some idea how this DNA (if it exists) would manage transposition steps 1-5.

Why not? What principle in molecular biology prohibits tsetse-fly DNA from appearing in tsetse-fly spit?

Tsetse fly DNA, were it injected into the bloodstream via the bite, WOULD NOT transpose.

wiki writes:Transposons work by copying themselves and pasting copies back into the genome in multiple places.

(Transposons) usually move by cut and paste, rather than copy and paste, using the transposase enzyme. Different types of transposase work in different ways. Transposase makes a staggered cut at the target site producing sticky ends, cuts out the transposon and ligates it into the target site. A DNA polymerase fills in the resulting gaps from the sticky ends and DNA ligase closes the sugar-phosphate backbone.

A common way of delivering transposons is to use a "suicide plasmid" that cannot replicate in the recipient cells.

Did you even bother to read the transposon link?

Now do you get it?

Blood-borne tsetse-fly genes might not be much different from the "imported sequences and mobile genetic parasites" that Frederic Bushman speaks of down at The Salk Institute. And he seems to be an expert on transposons.

No. You haven't explained yet how: "Our own DNA is a complex composite of imported sequences and mobile genetic parasites" (F. Bushman). You can't tell me how those mobile genetic parasites got into our DNA complex. You're saying it can't happen. But it did. Do you know more about this than Bushman does?

Roth and Wilson (1988) suggest that free chromosomal ends are generated from errors in DNA metabolism and at these sites segments of foreign DNA can integrate regardless of their terminal sequences. During this process, end-joining of multiple DNA fragments can occur.

Who's "wiki"? Wikipedia is not an authoritative source for this discussion. Did you even bother to read what Frederic Bushman said, quoted in Message 44?

These transposable elements transpose through a cut-and-paste mechanism; the element-encoded transposase catalyzes the excision of the transposon from its original location and promotes its reintegration elsewhere in the genome.

Autonomous members of a transposon family can express an active transposase, the trans-acting factor for transposition, and thus are capable of transposing on their own.

Nonautonomous elements have mutated transposase genes but may retain cis-acting DNA sequences necessary for transposition. These sequences, usually embedded in the terminal inverted repeats (IRs) of the elements, are required for mobilization in the presence of a complementary transposase.

Unfortunately, not a single autonomous element has been isolated from vertebrates; they seem to be defective for having mutations as a result of a process called “vertical inactivation”

HM writes:"Our own DNA is a complex composite of imported sequences and mobile genetic parasites"

wiki writes:At the most basic level, viruses consist of genetic material contained within a protective protein coat called a capsid. They infect a wide variety of organisms: both eukaryotes (animals, plants, protists, and fungi) and prokaryotes (bacteria and archaea). A virus that infects bacteria is known as a bacteriophage, often shortened to phage.

In eukaryotes, there are three general methods for entry into the cell. Some viruses are capable of uncoating merely by contact at the cellular membrane. In some cases binding of receptor triggers a process whereby a pore forms in the membrane between the inside of the capsid and the cytoplasm, causing the nucleic acid to enter the cell (Figure 5-4). In some enveloped viruses, the viral membrane fuses with the cell membrane, dumping the viral capsid into the cytoplasm. The capsid then uncoats releasing the nucleic acid. In the second general mechanism, viruses enter by utilizing uptake pathways normally used by the host for the transport of extracellular particles into the cell. This engulfment can be non-specific (phagocytosis) or, more typically, mediated by a receptor (endocytosis). In endocytosis, binding of a receptor by the virus particle causes it to migrate to a clathrin-coated pit, which is an area coated with protein (clathrin) that serves as a gathering point for transport of molecules into the cell. This triggers an invagination by the pit and the formation of a clathrin-coated vesicle. The vesicle uncoats by losing its clathrin and an endosome is formed. Proton-pumping proteins in the endosome membrane then cause a drop in pH. Finally, the endosome fuses with a lysosome and enzymes that degrade sugars, nucleic acids, proteins and lipids attack the contents of the vesicle. At all of these steps, viruses take advantage of the cells actions, using them as signals to initiate escape from the endocytotic pathway and invade the cytoplasm. These signals cause the virus to inject its nucleic acid into the cytoplasm in a fashion somewhat similar to that used by most bacterial viruses.The third method of entry to a eukaryotic cell involves the intact virus being endocytosed, but instead of just the nucleic acid entering the cytoplasm, the entire virus does. The virus then triggers lysis of the endosome membrane and enters the cytoplasm intact. Viral uncoating then occurs at the nuclear membrane.

But you still have along way to got to make any sort of case that such a mechanism is required or indeed that there is anything to be explained.

Then genes can hop onto those cabooses of terminal sequences.

Must carefully REGULATE entry.Ordinary genomic DNA is not capable of regulating entry into a cell.HM. Look in the index of Bushman's book. Find "transposition" or "method of transposition" and you will see that I am right.

transfer to the nucleus has been suggested to be facilitated by transposable or viral elements because of their proximity to many numtDNA sequences.

The mitochondrial genome indicate that fragments join together from an intracellular pool of RNA and/or DNA before they integrate into the nuclear genome.

On its course through the body, the food-vacuole usually decreases greatly in size, and the acidity of its content increases greatly; the acidity ... increases to a maximum at least as high as pH 1.4 and then decreases approximately to pH 7.8.

DNA under physiological conditions has been estimated to depurinate at a rate of 3 x 10e11/sec at 37C and pH 7.4

Depurination involves the loss of purine bases forming abasic sites

Amines greatly increase the rate of strand breakage at abasic sites

Suddenly the tenuous connection you were drawing, with no evidence to support it, is supposed to be expert opinion from Bushman? The incorporation of viral sequences or sequences from organelles both involve genetic sequence already on the inside of the cell membrane and either present or capable of propagating to cells throughout the body.There is no need for some magical route for DNA from a tsetse cell in saliva to be incorporated into the genomic DNA of a gamete in order to explain Bushman's statement, just the known factors such as retroviral insertion and transposase activity.

Roth and Wilson (1988) suggest that free chromosomal ends are generated from errors in DNA metabolism and at these sites segments of foreign DNA can integrate regardless of their terminal sequences. During this process, end-joining of multiple DNA fragments can occur.