Non-mendelian genetics/ non-darwinian evolution

I agree with this. My thoughts would be that
1) Species imprinting could contribute to differential expression of coding/non-coding between species that share significant nucleotide homology and explain the tolerated accrual of mutations one sees in the non-coding sections of human DNA by setting the stage for this differential methylation/acetylation you were suggesting as a species block...maybe. Where the focus is conservation of specific species. - Then the parental imprinting, much more plasticity involved, where the imprinting of heritability affected by environment (oocyte, in utero, nuclear, take your pick) but again not in a mendelian fashion, but in addition to mendelian genetics. I think that is what you were already saying though (right?). The focus would be conservation of organism function (whatever level that might be).So, a tri-level approach (species imprinting, parental imprinting, and mendelian genetics) to getting to the point that you and I are discussing this (of course that simple ). Maybe this was what you were suggesting as well? I hope I managed to make sense since my communication skills seem to wane at times.

You know what, lol, I'm calling a truce. I think somewhere the gist if what I had meant to say in the first post has gotten lost. We are not getting any further and we have digressed to picking at small things, and I do mean 'we', so have a great week .-Cheers

I just had my attention drawn to a new paper in 'Genes & Development' on an apparent induction of stable epigenetic inheritance in flies. It isn't totally clear how distinct this mechanism is from other previously noted epigenetic modifications localised to chromatin restructuring or methylation but it has been induced in a novel way.TTFN,WK

I'm a bad lazy person and I never got around to properly writing up my thoughts on this topic. Nevertheless I thought I might bump this thread since a new and interesting 'non-mendelian' paper has come up. The paper is being discussed in the 'Mendel wasn't entirely right' thread, whose originator seems to be under the impression that Mendelian genetics is both the be all and end all of genetics and some sort of keystone of all evolution, so I thought a little reminder of the other factors known to mediate inherited characteristics would be worthwhile.TTFN,WK

All life, including us, were created by scientists from another planet. As you can see, life can not evolve random, someone has to interact to create these new lifeforms. To read more, go to rael.org and check out a free e-book.

You are doing a bit too much pushing of your favourite site. This is a discussion forum.I suggest you restrict yourself to one or two discussions. If you wish to make claims of what you consider fact in them you will have to support your claims. This support will have to be posted here with both evidence and reasoning.If you continue to post as you have been I will have to suspend your posting priveldges for a period of time.

More epigenetic inheritance research, this time from Science. So this methylation based male infertility has been heritable over 4 generations.TTFN,WK

Another non-mendelian example probably related to epigenetic factors. In mice again and this time associated with tail colour (Rassoulzadegan, et al., 2006). TTFN,WK

Most aphid species carry obligate symbionts in the form of various strains of the bacterium Buchnera aphidicola. The bacteria cannot survive outside the aphid and the aphid relies on them to synthesize various amino acids (usually trypotophan) that it cannot produce for itself. The bacteria are housed in a special cellular organelle, a bacteriocyte, and are inherited vertically - every developing aphid embryo receives symbionts through special processes growing from neighboring maternal bacteriocytes.Things got more interesting with the discovery of a series of 'secondary' aphid sympbiotes belonging to various other bacterial genera. These are not completely essential for aphid survival, but some provide the aphid with interesting and unique phenotypic abilities (new host range, change in thermal tolerance, etc.). Cytological studies have revealed these bacteria 'piggy-backing' on the bacteriocytes of the primary symbionts to ensure their inheritance, although they are not actually housed within them (yet?) and their inheritance is not as consistent (usually less than 100%).So my question is, would you consider the vertical inheritance of such symbionts to constitute a valid form of epigenetic inheritance, at least relative to the genome of the aphid ?I guess we first have to decide whether the symbionts still deserve status as separate organisms, or whether the aphid+symbionte can be considered 'all one organism' at this point, in which case I guess the answer would be 'yes'.

I'd be inclined to count this as a form of cytoplasmic inheritance if the bacteria aren't actually enclosed in the bacteriocyte.Actually looking at some of the literature it seems that rather than an organelle, unless you are using this in an unusual way, the bacteriocytes are actually specialised cells (Braendle, et al., 2003).It sounds quite similar to the maternal transmission of acquired immunity to me. I'd definitely tend to consider this a valid example of epigentic inheritance, akin to mitochondrial inheritance but on an organismal rather than cellular level.TTFN,WKEdited by Wounded King, : for comprehensibility

Yes, my incorrect terminology. The Buchnera are fully enclosed by special cells.I think it's fascinating that these secondary endosymbiontes are now jockeying for position (competing?) with the more ancient Buchnera for a position within the aphids. Organisms can be viewed as composite micro-ecosystems.Incidentally, the genetic phyllogeny of the Buchnera complex has a wonderful congruency with the genetic phylogeny of the Aphididae and various novel acquisition events can be inferred in different aphid lineages.