Molar Pregnancies and Genome Imprinting

[Petrel]

So the forum lately has been hijacked for theistic evolutionist bashing, so I'm posting a thread to get things back on track.

A few years ago I found myself wondering--why does a molar pregnancy not involve an embryo?

For those who don't know about this, a molar pregnancy (hydatidiform mole) occurs when an egg somehow ends up without its maternal DNA. When it is fertilized it contains only half of the DNA needed. This paternal DNA then copies itself, so the zygote formed contains the 46 chromosomes we need for development. Assuming the sex chromosome contributed by the father is X, the zygote should grow into a baby girl. However, then development goes drastically wrong. Instead of dividing and growing to form the embryo and the placenta needed to feed it, it divides and starts forming beads of placenta-like tissue. This tissue may become invasive and cause a type of cancer called a choriocarcinoma. The usual treatment once molar pregnancy is diagnosed is curettage to remove the abnormal tissue and sometimes even hysterectomy.

This is a complete hydatidiform mole, there is also a partial hydatidiform mole caused by two sperm fertilizing one egg to produce a triploid (69n) zygote, but it makes immediate sense that that would not be viable.

No source that I read talked about the reason for this at all, so I turned to journals. I ran across an article involving experiments with mice where they made zygotes containing either all paternal DNA or all maternal DNA. When all maternal DNA was used, the embryo began development normally, but the placenta did not form and the embryos eventually died. When all paternal DNA was used, the case was similar to that of a complete mole--placenta-like tissue proliferated, but the embryo did not form.

It ends out that the reason for this difference is a process called genome imprinting. Imprinting in mammals involves patterns of DNA methylation. Not much is known about imprinting, and it serves different roles at different times of development. When gametes are formed their DNA is methylated in a different fashion depending on whether they are eggs or sperm. When they combine, the methylation pattern of each DNA duplex determines whether its genes are used in the growth of the placenta or the embryo. During embryo growth, the genome imprinting of the maternal and paternal DNA is erased and then the embryo re-methylates the DNA in a manner that permits proper transcription control for that point in development.

Here is a page that talks more about genome imprinting and its significance.

 

[Deacon]

I sure hope your interest wasn’t due to any personal involvement.

One of my hobbies is the propagation of daylilies.

A “normal” daylily has 22 chromosomes (receiving 11 from the egg, and 11 the sperm cells).
By using colchicine (a natural occurring toxin from the autumn crocus) you can produce triploid (33) and tetraploid (44) plants.

Triploid daylilies are sterile; the gametes can’t divide equally in half (technically it’s possible but it’s like the average American family of 2.2 children; you can’t find one).

Now occasionally a variant occurs when a diploid daylily producing unreduced gametes (22 gametes in the egg or pollen cell) is crossed with a tetraploid daylily (containing 44 chromosomes), (…so you have 22 gametes crossing with 22 gametes)…ending up with a fertile match (44 chromosomes) walla, a new type of tetraploid daylily.

What’s the advantage for the daylily enthusiast? More chromosomes equal more information resulting in thicker, stronger daylilies with more color variations.

Fortunately once produced (and deemed worthy), these daylilies are propagated through division of their roots.

Rob

 

[Petrel]

No, fortunately, I imagine that would be as upsetting as a miscarriage and possibly worse if there was fear of cancer. I first ran across a detailed discussion of this in one of my friend's nursing books in college, but they didn't explain the role of genome imprinting. I thought about it again several years later when I was doing some reading about chromosome abnormalities.

It's interesting how polyploidy plays such a role in the development of new plant species, but it's almost always a fatal event in animals. However, I believe Uteotw posted some evidence before that radiation of an ancestral tetrapod followed a polyploidy event. It would have been interesting to watch that occur. I will try to look it up later if I have time.

 

[Petrel]

It ends out that fish tend to go polyploid all the time!

"Occurrence of polyploidy in the fishes." Leggatt, R.; Iwama, G. Reviews in Fish Biology and Fisheries, 2003, 13, 237-246.

Changes in chromosome numbers and genetic material have played a determining role in the evolution of eukaryotic life. The most dramatic change probably occurs through a process known as polyploidy, or the multiplication of the entire genome or sets of chromosomes. Polyploidy is a widespread phenomenon within the plants and has appeared sporadically throughout the animal kingdom. Two genome-doubling events are considered to have taken place before the tetrapods split from the fish 360 million years ago (mya; Allendorf and Thorgaard, 1984; Wittbrodt et al., 1998; Zhou et al., 2002), resulting in an ancestral diploid chromosome number (2N) of approximately 48. While uncommon in higher vertebrates, polyploidy has appeared repeatedly during the development and diversification of the fishes, from the sharks to the higher teleosts. Many economically important fish, such as carp, salmon and sturgeon, have evolved from polyploid ancestors. As well, artificially-induced polyploidy has been used in aquaculture to produce sterility or improve production (Donaldson and Devlin, 1996). Although the majority of fish have a 2N of approximately 48 (Stingo and Rocco, 1991), chromosome numbers of 100, 150, and over 400 exist.

There appears to be a specific advantage of polyploidy due to having additional copies of genetic code. In diploid fish, randommutations of alleles performing essential roles in the survival of an organism would have deleterious effects on the organism, but additional copies of the allele in polyploid fish would decrease the probability of such negative effects (Ohno, 1970; Wittbrodt et al., 1998). This could allow the genes to diverge in function, as observed in the catastomid and salmonid fishes (Ferris and Whitt, 1979; Allendorf and Thorgaard, 1984), or result in differential expression through the organism and during development (Aparicio, 2000). While the divergence of duplicate genes is well discussed in the literature (Ohno, 1970; Ferris and Whitt, 1979; Li, 1980; Allendorf and Thorgaard, 1984; Larhammar and Risinger, 1994; Wittbrodt et al., 1998; Aparicio, 2000; Otto and Whitton, 2000; Taylor et al., 2003), this represents a process that takes place in established polyploid species (Li, 1980). The immediate advantages of increased copies of alleles to the establishment of a polyploid fish are not well known. It has been suggested that polyploid organisms may gain an advantage by increased expression of key physiological proteins due to increased numbers of genes, such as the a-gonadotroponin gene in the goldfish (C. auratus; Ferris, 1984; Larhammar and Risinger, 1994). However, the increased genetic material in polyploid cells increases the overall cell size in polyploid individuals. As the majority of polyploid fish do not differ in body size from their diploid relatives, there is an overall decrease in cell number and in cell surface area to volume ratio in these fish (Benfey, 1991, 1999). Hence, the overall numbers of genes in the organism are not greatly affected by polyploidy and an overall increased expression of proteins is unlikely in polyploid fish. Immediate advantages of duplicate genes in the establishment of polyploid fish are not yet clear.

I expect that polyploidy may be more common in amphibians and reptiles than I expect as well, and I will look into this.