Thursday, 11 December 2025

Creationist Blasphemy and the Mammalian Placenta

 Creationist Blasphemy and the Mammalian Placenta:
The facts surrounding the genetics of placental formation.


https://docs.google.com/document/d/1862O6Vme0UXNEl-XsCHRkC3Oh3Vn3Ab3YQAesUEqM2c/edit?usp=sharing 



In their desperation to try to question the proof of evolution, beyond any reasonable doubt that endogenous retroviruses (ERVs) provide, creationists will bleat that their intelligent designer - sorry, Intelligent Designer - or ”God” - created specific genes of only seemingly retroviral origin that are essential in the formation of the placenta in mammalian species, including us.

This, they consider, is their most powerful rebuttal. It comes up so frequently, with an air of certainty and triumph.

These genes are the genes for forming the placental syncytiotrophoblast, a syncytium, a single cell formed by the fusion of cells with multiple cell nuclei. The genes responsible for their formation are called syncytins.


They argue that placental species could not have survived without these genes. Indeed, if they are “knocked out” in experimental mice, for example, those mice are rendered incapable of producing offspring.

How could the ancestors of mice have ever thrived before they could produce placenta to produce offspring?

This is an example of the fallacious reasoning behind “irreducible complexity”, the distorted rip-off of the evolutionary concept of interlocking complexity described by H. L. Muller in the earlier part of the 20th century. Elements may arise and subsequently become indispensable.


The devil, as they say, is in the details, which are typically glossed over (usually ignored) by creationist firefighting hacks writing about ERVs and placentae. Syncytins are to be found in ERVs, in exactly the same genetic context as retroviral envelope (env) genes. They are, essentially, env genes. Env genes are responsible for targeting and attaching the virus to specific cell types, and to infiltrate the target cell membrane.

“Evolutionists” (non antisci creationists/intelligent designer spotters) argue that syncytins are derived from the env genes of retroviruses that have endogenized in host genomes.

HIV is known to create syncytia by virtue of its env gene in its evolutionary battle with host T-cells by getting infected cells to “swallow” them. HIV is not known to have endogenized in any organism’s genome. This argues that syncytins are a part of the “design” of retroviruses, rather than of original host genomes.

Here is why we conclude - not “claim”, not “guess”, certainly not “presuppose”, 

that ERVs are of retroviral origin: 


https://barryhisblog.blogspot.com/p/why-do-virologists-and-geneticists.html
The full ERV FAQ is linked to at the top of the page.

The fact that syncytins found in ERVs are involved in other types of tissues, other than placentae, also proves that they were not “designed” just for the purpose of creating placentae.

The fact that different placental lineages use different syncytins from different ERVs, on different chromosomes, puts paid to the “same design, same designer” (sorry, Designer) argument.

The fact that some placental lineages do not use syncytins at all puts paid to the argument that they are or always were necessities.

The fact that particular syncytins in particular ERVs appear in the same lineages provides additional proof of evolutionary relatedness within lineages.












Syncytins in other tissues



1. Expression in Non-Placental Normal Tissues

  • Low/weak expression in some reproductive tissues such as endometrium, ovary, and testis has been reported in humans, although at much lower levels than in the placenta and with unclear functional significance. ScienceDirect

  • Some studies have detected very low syncytin transcript levels in brain tissue of mice outside of the placenta, but these are minor relative to placental expression. Sujet de Bac

2. Roles in Muscle Development

  • In mice, endogenous retroviral envelope genes captured as syncytins contribute to myoblast fusion — a process by which mononuclear muscle precursor cells fuse to form multinucleated myofibers.
    Knockouts of certain syncytin genes result in reduced muscle mass and fewer nuclei per fiber, particularly noticeable in males, indicating a role beyond placentation in normal development. PubMed

3. Osteoclast and Cell Fusion Processes

  • Some research indicates syncytin expression is associated with cell–cell fusion in osteoclast precursors (bone-resorbing cells). This suggests a function in bone physiology where cell fusion is important. cjcr.amegroups.org

4. Expression in Pathological/Transformed Cells

  • Syncytins have been detected at higher levels in various cancer cells compared with normal somatic tissues — including breast cancer, endometrial cancer, ovarian cancer, and leukemia. Their expression in tumors is being investigated for possible effects on tumor progression, prognosis, or cell fusion phenomena in cancer. ScienceDirect+1

  • Syncytin expression has also been noted in autoimmune conditions such as multiple sclerosis, though the significance of this is controversial and under study. cjcr.amegroups.org

5. Syncytin-like Genes in Other Vertebrates

  • Syncytin homologs with fusogenic roles also occur in non-mammalian species with placental-like structures (e.g., viviparous lizards), indicating that capture of retroviral env genes can be co-opted for tissue fusion in diverse contexts, but their expression outside reproductive tissues in these species is less well characterized. PubMed



Placental mammal lineages 

Mammalian Group

Known Syncytin Genes

Origin (ERV lineage)

Placental Type / Notes

Primates (humans, apes, monkeys)

Syncytin-1, Syncytin-2

Independent retroviral env genes (HERV-W, HERV-FRD)

Highly syncytial hemochorial placenta

Rodents (mice, rats)

Syncytin-A, Syncytin-B

Distinct murine endogenous retroviruses

Hemochorial placenta; both required for syncytiotrophoblast fusion

Lagomorphs (rabbits)

Syncytin-Ory1

ERV of independent origin

Hemochorial placenta

Carnivores (cats, dogs)

Syncytin-Car1 (and possibly others)

Distinct ERV origin

Endotheliochorial placenta (less invasive)

Ruminants (cows, sheep, goats)

Syncytin-Rum1 (sheep/goat), Syncytin-Bos1 (cow)

Independent ERVs

Synepitheliochorial placenta (limited fusion)

Bats (Chiroptera)

Multiple lineage-specific syncytins (e.g., Syncytin-Peg1, Syncytin-Chi)

Several independent ERV captures

Hemochorial or endotheliochorial, depending on species

Afrotherians (elephants, hyraxes, manatees)

No known syncytin identified

Hemochorial (elephant) or epitheliochorial (manatee) placentas; fusion mechanism unknown

Xenarthrans (armadillos, sloths)

No known syncytin identified

Variable placentas; may have limited or no syncytiotrophoblast layer

Eulipotyphlans (shrews, moles)

Syncytin-Slu (in shrews)

Independent ERV origin

Hemochorial placenta

Tenrecs, aardvarks, others

No syncytin detected yet

Likely rely on alternative mechanisms

Why “blasphemy”?


As we have seen, all the facts point to syncytins having originated in endogenizations of retroviruses, and are therefore not genes “designed” into their carriers’ genomes.

What is blasphemous about continuing to try and insist that they were designed into our genomes?

Well, you would have to say that your designer - sorry, Designer - must have put all this detailed evidence in our genomes, falsely, and unnecessarily, apart, that is, from having the motive of trying to lead us astray.  It would be like Loki, the wizard of lies. The “Designer” is not supposed to be a liar and deceiver. Either it is, and it faked the evidence, or it didn’t, and all the implications from ERVs for evolution are real.

It would be quite a puzzle, why would it engage in a subterfuge that would only target us once we had figured out DNA and RNA and viruses and all this stuff? Did the people who lived before all these discoveries not need to be fooled into thinking we evolved? Why the elaborate fake evidence to fool just us? What for? This would be dark, insane mischief, for sure., yet this is effectively what you believe your “Designer” is like, if you are an antisci conspiracy theorist.
 

References


Carter, A. M. (2001)

Carter, A. M. (2001). Evolution of the placenta and fetal membranes seen in the light of molecular phylogenetics. Placenta, 22(10), 800–807. PubMed: 11718566

Carter, A. M. & Mess, A.

Carter, A. M. & Mess, A. (2007). Evolution of the placenta in eutherian mammals. Placenta, 28(4), 259–262. DOI: 10.1016/j.placenta.2006.04.010 portal.findresearcher.sdu.dk

Carter, A. M. & Enders, A. C.

Carter, A. M. & Enders, A. C. (2004). Comparative aspects of trophoblast development and placentation. Reproductive Biology and Endocrinology, 2, 46. DOI: 10.1186/1477-7827-2-46 BioMed Central

Wildman, D. E. et al.

PNAS, DOI: 10.1073/pnas.0511344103.

Murphy, W. J. et al. (2021)

Annual Review of Animal Biosciences, DOI: 10.1146/annurev-animal-061220-023149.

Dupressoir, A. et al. (2009)

PNAS, 106(29), 12127–12132. DOI: 10.1073/pnas.0406509102

Dupressoir, A. et al. (2011)

PNAS, 108, E1164–E1173. PubMed: 22032925

Mi, S. et al. (2000)

Nature, 403, 785–789. DOI: 10.1038/35001608

Blaise, S. et al. (2003)

PNAS, 100, 13013–13018. DOI: 10.1073/pnas.2132646100

Cornelis, G. et al. (2012)

PNAS, 109(11), E432–E441. DOI: 10.1073/pnas.1115346109

Cornelis, G. et al. (2013)

PNAS, 110, E828–E837. DOI: 10.1073/pnas.1215787110

Cornelis, G. et al. (2014)

PLoS Genetics, 10(11), e1004098.  PLoS Genetics.) DOI: 10.1371/journal.pgen.1004098

Varela, P. et al. (2015)

Viruses, 7(6), 2753–2770. DOI: 10.3390/v7062753

Heidmann, O. et al. (rabbit)

Heidmann, O., Vernochet, C., Dupressoir, A., & Heidmann, T. (2009). Identification of an endogenous retroviral envelope gene … in rabbit. Retrovirology, 6, 107. DOI: 10.1186/1742-4690-6-107 pmc.ncbi.nlm.nih.gov

Esnault, C. et al. (2013)

Esnault, C., Cornelis, G., Heidmann, O., & Heidmann, T. (2013). Differential evolutionary fate of an ancestral primate endogenous retrovirus envelope gene … PLOS Genetics, 9(3), e1003400. DOI: 10.1371/journal.pgen.1003400 pmc.ncbi.nlm.nih.gov


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