Long silent time. Not caused from any shortage of coffee or interest about science but the last few years my life have been quite weird. The revival of this blog should be short, just to discuss a few points about memetics.
During a 24h vacation from my actual preoccupations I came across a paper from Maarten Boudry (get a copy here) :
Replicate after reading: on the extraction and evocation of cultural information
Maarten Boudry, Biology & Philosophy (2018) 33:27 https://doi.org/10.1007/s10539-018-9637-z
My interest was triggered by a tweet: — Maarten Boudry (@mboudry) July 11, 2018
Old joke presented here and there are a few variants about its conclusion. I have use it to illustrate how the same stimulus may elicit different responses depending on the system under investigation and its receptors, say doxycycline used for expression of a transgene under a TetOn promoter and the role of the antibiotic on angiogenesis inhibition; that may be tricky if your transgene is also supposed to inhibit angiogenesis, right?
Anyway, I got a copy of Boudry’s paper and I started reading. The way I used the joke is contradicting the assertion on page 26:
For the system to work, every participant already needs all the jokes stored in memory, along with the corresponding numbers. This, of course, is the point of the punch line: if you start laughing, you must have heard the joke before.
Another Real World example to support my objection.is the evolution of the metabolic pathways producing THC; they didn’t evolve for recreational or medical use, right? Same stimulus, different receptor, different effect.
But that’s something to discuss about and it’s fun to start discussing about jokes. I’ll put that aside, maybe for later.
But than Boudry starts discussing about Sperber and on page 27 he cites from Sperber D (2000) An objection to the memetic approach to culture. In: Aunger R (ed) Darwinizing culture: the status of memetics as a science. Oxford University Press, Oxford, pp 163–173
In general terms, Sperber proposes three “minimal conditions for true replication”. For B to be a copy of A,
- B must be caused by A (together with background conditions)
- B must be similar in relevant respects to A
- The process that generates B must obtain the information that makes B similar to A from A.
Now, when you talk about true replication to a biologist you have his attention. Instantly. Of the various types of biological replication my favorite is the rolling circle some bacteriophages use. And it is used also for in vitro isothermal amplification. Certainly not the most common one, so I’ll stick with the more used one here.
Let’s examine the three points Sperber proposes for B to be a copy of A and if it’s possible to qualify DNA replication as true.
Point 1 is OK I think if we take in the background conditions the DNA polymerase, the dNTPs and a bunch of other stuff. I singled out the enzyme and the dNTPs because I want to discuss them below.
Point 2 is problematic. In fact, from a double stranded DNA molecule A we can obtain two double stranded DNA molecules indistinguishable from A (no mutations for the moment and the necessary machinerie to polish the ends of the molecules.) During the replication process, the DNA polymerase synthesise two DNA strands that are the reverse complement of the strand serving as matrix!
Because the two strands of the initial DNA molecule are antiparallel and each one the reverse complement of the other, because of that and only because of that, the two final molecules are similar. And the DNA replication being semi-conservative each of the two resulting molecules is composed by half of the initial one!
So, according to point 2 of Sperber’s DNA replication is not a true replication. I think that Meselson–Stahl or Crick-Watson would be quite sad to learn that.
Is it necessary to go to point 3? Probably not, we already know that we are in a GIGO situation here. But just for the fun of it and maybe for future use in a more appropriate set of rules let’s examine how the DNA polymerase knows what must be the next base to incorporate in the neosynthetised strand: it doesn’t.
The complementary base, able to establish the adequate number of hydrogen bonds with the one of the template (A::T or C:::G) will be correctly positioned to allow the catalysis of its incorporation. The DNA polymerase only sees that it is able to catalyse the formation of a new phosphodiester bond. That’s quite convenient when you need to incorporate to the neosynthesised strand some nucleotide analog, using say dig-dUTP an analog of TTP. And such altered DNA strands may be used as matrices to produce more canonical reverse complements later on.
So, what would true replication be?
We surely have information transfer from one object to other objects, in the case of DNA replication discussed above in the two resulting double stranded molecules. In other systems we may have transfer of the information in several other molecules. That’s what I like in the rolling circle replication system where a single matrix molecule is used to produce hundreds of daughter (reverse complement) strands each of them circularised and encapsulated in a virion in the replication of say filamentous phages.
Some times the information is stored in a similar medium (say DNA or RNA or PNA). Or it can be stored in a completely different medium: for genetic information in silico instead in carbon based molecules. I salute here Craig Venter and his team who brought us the proof of concept. So, the nature of the support doesn’t matter. Sperber’s point 3 is pertinent here, but still not point 2.
I can’t imagine anything else to define a true replication. Maybe you do and the comments are open.
But I suggest that Sperber’s definition should be respectfully discarded and not used in memetics as it can’t be used in biology.
Vertebrate limbs first emerge as small buds at specific locations along the trunk. Although a fair amount is known about the molecular regulation of limb initiation and outgrowth, the cellular events underlying these processes have remained less clear. We show that the mesenchymal limb progenitors arise through localized epithelial-to-mesenchymal transition (EMT) of the coelomic epithelium specifically within the presumptive limb fields. This EMT is regulated at least in part by Tbx5 and Fgf10, two genes known to control limb initiation. This work shows that limb buds initiate earlier than previously thought, as a result of localized EMT rather than differential proliferation rates.
Gros J, Tabin CJ.
Science 14 March 2014: Vol. 343 no. 6176 pp. 1253-1256, doi:10.1126/science.1248228
D’abord, cartes sur table, je travaille pour Portable Genomics Inc., une société américaine, démarrée par des francais éxilés aux USA (à cause de l’ineptie qu’est la loi bioéthique française), et dont le business est lié cet espace de la génétique et de la génomique personnelle.
Avant une dissection en règle de cette mise au point deux choses que je souhaite clairs :
– Effectivement, la médecine, ce n’est pas le tiercé. Je suis entièrement d’accord.
– La génétique personnelle n’est pas le tiercé non plus; elle demande des médecins capables d’exploiter les connaissances actuelles et justement, pour éviter le tiercé, je ne laisserai jamais un médecin comme Munnich s’occuper de moi ou des gens auxquels je tiens.
NDE have been used as proof of the existence of souls in a large set of stupid arguments.
Following this trend, it seems that prophet Sir Terry Pratchett revealed that rats have souls, managed by the DEATH of Rats of course, in his novels.
Now scientific evidence come to support either:
- the existence of rats’ souls, or
- the non-supernatural, quite materialistic, explanation of NDE.
Jimo Borjigin, UnCheol Lee, Tiecheng Liu, Dinesh Pal, Sean Huff, Daniel Klarr, Jennifer Sloboda, Jason Hernandez, Michael M. Wang, and George A. Mashour
Surge of neurophysiological coherence and connectivity in the dying brain
PNAS 2013 ; published ahead of print August 12, 2013, doi:10.1073/pnas.1308285110
The brain is assumed to be hypoactive during cardiac arrest. However, the neurophysiological state of the brain immediately following cardiac arrest has not been systematically investigated. In this study, we performed continuous electroencephalography in rats undergoing experimental cardiac arrest and analyzed changes in power density, coherence, directed connectivity, and cross-frequency coupling. We identified a transient surge of synchronous gamma oscillations that occurred within the first 30 s after cardiac arrest and preceded isoelectric electroencephalogram. Gamma oscillations during cardiac arrest were global and highly coherent; moreover, this frequency band exhibited a striking increase in anterior–posterior-directed connectivity and tight phase-coupling to both theta and alpha waves. High-frequency neurophysiological activity in the near-death state exceeded levels found during the conscious waking state. These data demonstrate that the mammalian brain can, albeit paradoxically, generate neural correlates of heightened conscious processing at near-death.
Illustration by ~Smaggers
Guillaume Andrey, Thomas Montavon, Bénédicte Mascrez, Federico Gonzalez, Daan Noordermeer, Marion Leleu, Didier Trono, François Spitz, Denis Duboule
Science 7 June 2013: Vol. 340 no. 6137 dpi: 10.1126/science.1234167
During limb development, the time and place of Hox transcription are fixed by respective gene position within the gene cluster. Andrey et al. (p. 1234167; see the Perspective by Rodrigues and Tabin) found that this enigmatic property results from the opposite and successive actions of two large regulatory landscapes located on either side of the mouse Hox locus. In the early phase, one of these topological domains regulates transcription in the proximal limb until a switch occurs toward the other topological domain, which takes over the regulation in the distally developing digits. As a side effect of this antagonistic regulatory strategy, cells in-between have lessened Hox transcription, which generates the wrist.
Sequencing of the sea lamprey (Petromyzon marinus) genome provides insights into vertebrate evolution
Sequencing of the sea lamprey (Petromyzon marinus) genome provides insights into vertebrate evolution
Smith JJ, Kuraku S, Holt C, Sauka-Spengler T, Jiang N, Campbell MS, Yandell MD, Manousaki T, Meyer A, Bloom OE, Morgan JR, Buxbaum JD, Sachidanandam R, Sims C, Garruss AS, Cook M, Krumlauf R, Wiedemann LM, Sower SA, Decatur WA, Hall JA, Amemiya CT, Saha NR, Buckley KM, Rast JP, Das S, Hirano M, McCurley N, Guo P, Rohner N, Tabin CJ, Piccinelli P, Elgar G, Ruffier M, Aken BL, Searle SM, Muffato M, Pignatelli M, Herrero J, Jones M, Brown CT, Chung-Davidson YW, Nanlohy KG, Libants SV, Yeh CY, McCauley DW, Langeland JA, Pancer Z, Fritzsch B, de Jong PJ, Zhu B, Fulton LL, Theising B, Flicek P, Bronner ME, Warren WC, Clifton SW, Wilson RK, Li W.
Nat Genet. 2013 Apr;45(4):415-21, 421e1-2. doi: 10.1038/ng.2568. Epub 2013 Feb 24
Sea lamprey mouth (Photo: T. Lawrence, GLFC)
Macrophages are required for adult salamander limb regeneration
James W. Godwina, Alexander R. Pinto, and Nadia A. Rosenthal
Published online before print May 20, 2013, doi: 10.1073/pnas.1300290110
Neural Decoding of Visual Imagery During Sleep
T. Horikawa, M. Tamaki, Y. Miyawaki, Y. Kamitani
Science 3 May 2013: Vol. 340 no. 6132 pp. 639-642 doi: 10.1126/science.1234330