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Origin of homochirality in an early peptide world Axel Brandenburg, Harry Lehto and Kirsi Lehto (Nordita) Int. J. Astrobio. 3, 209 (2004), 4, 75 (2005),

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Presentation on theme: "Origin of homochirality in an early peptide world Axel Brandenburg, Harry Lehto and Kirsi Lehto (Nordita) Int. J. Astrobio. 3, 209 (2004), 4, 75 (2005),"— Presentation transcript:

1 Origin of homochirality in an early peptide world Axel Brandenburg, Harry Lehto and Kirsi Lehto (Nordita) Int. J. Astrobio. 3, 209 (2004), 4, 75 (2005), Orig. Life Evol. Biosph. 35, 225 (2005), 35, 507 (2005) Some advantages of peptide world Plasson et al. model: is non-autocatalytic Is this true? How come? Connection with earlier work Plasson model is auto-catalytic in some sense!

2 2 Producing enantiomeric excess (e.e.) Life only develops in homochiral environment –Isotatic chains more stable –Homochirality is a prerequisite –Amino acids in dead organisms lose e.e. However: no mechanism produces 100% e.e. –only minute partial excess possible (electroweak) –slightly bigger for large Z, goes like Z 5  Cu (II) ions Still need amplification mechanism –Frank (1953) model (plus extensions): nucleotides –Autocatalysis and enantiomeric cross inhibition –Plasson, Bersini, Commeyras (2004): peptides

3 3 Chirality selection during polymerization of the first replicating molecule? R L Isotactic polymer (same chirality) “waste” (enantiomeric cross-inhibition) dual world RNA world Peptide world, PNA world lipid world? RNA RNADNA proteins Rasmussen et al (2003 Artif. Life 9, 269-316) achiral chiral Monomers to dimers

4 4 RNA versus peptide worlds Activation D  D*, L  L* Polymerization D+D  DD, L+L  LL Epimerization DL  LL, LD  DD Depolymerization DD  D+D, LL  L+L Template-directed (PCR-like) Enantiomeric cross- inhibition Autocatalytic production of new mono-nucleotides (  but uncertain) RNA world peptide world APED model (Plasson et al.)

5 5 Recap of Frank-type model (Frank 1953) auto-catalysis alone kinetic equation enantiomeric excess: exponentialgrowth catalyst

6 6 Need mutual antagonism add cross-inhibition kinetic equation unspecific antagonism

7 7 APED model (Plasson et al. 2004) e: epimerization on N-terminal DL  LL not DL  DD a: activation p: polymer.  : inhibition h: depolym.

8 8 APED model equations Consider limit of large h and e

9 9 APED model equations limit of large h and e corresponding reaction  D catalyzes conversion of both D* and L* into D

10 10 Reduced APED model a one way round-about For nearly racemic state:

11 11 Exponential evolution For nearly racemic state:

12 12 Conclusions Plasson et al. model is simple No explicit autocatalysis necessary Autocatalytic (autoinductive) effects can be identified Experiments now necessary

13 13 Initial bias not necessary Exponential amplification Initial excess can be virtually zero Initial bias may not change this –depends on strength Second genesis: other chirality? –would be cool –but is not necessary Bifurcation diagram fidelity with Andersen, Höfner, Nilsson Orig. Life Evol. Biosph. 35, 225 (2005)


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