This site is not maintained. Click here for the new website of Richard Dawkins.

JJFinch's Profile

JJFinch's Avatar Joined almost 4 years ago
Gender: Female

Latest Discussions Started by JJFinch

More Discussions by JJFinch

Latest Comments by JJFinch

Go to: ‘How do atheists find meaning in life?’

JJFinch's Avatar Jump to comment 163 by JJFinch

Excellent article, and the paper that is linked to is also a fantastic and fascinating (though not at all surprising) read. I took some of the most pointed excerpts from it and put them together in a note on facebook for any of my friends inclined to believe that atheists have no meaning or values in their life. :)

Fri, 20 Jan 2012 16:51:18 UTC | #910205

Go to: Stupid and clever questions for people who understand the biology

JJFinch's Avatar Jump to comment 62 by JJFinch

@NealOKelly

"Darwinism, in its modern form, expects that individuals will strive to pass on as many of their genes as possible. So, isn't it just daft to throw half your genes away with every sperm you make, in order to mix the other half with genes of somebody else?

...

"The widespread existence of males who don't earn their keep as fathers must mean that there really are very substantial Darwinian benefits of sexual recombination itself. It's not too difficult to think of what they might be in qualitative terms, and lots of possible benefits, some obvious, some esoteric, have been proposed. The problem is to think of a benefit of sufficient magnitude to counteract the massive... cost.

There are a number of benefits to sex, which I studied in my evolution course last year, but my mind's blanking and I can't remember any except: Sexual reproduction produces more variable offspring and, as the conditions of life are variable, sex therefore provides a greater chance that some among ones offspring will be better adapted to the current environment. (I don't have my notes from last year with me either)

I do remember that sexual populations are able to evolve faster than asexual ones because beneficial mutations can come together simultaneously from two different lineages, they don't have to be acquired sequentially in one lineage. However this is a long-term benefit, and natural selection could not (I think) act on this.

There is also (it's starting to come back to me) something to be said about resistance to disease or parasites - if all of your offspring are identical to you (and therefore each other) then something like a disease or parasite that is capable of killing you is likely to kill all your offspring, whereas this may not be the case if you reproduce sexually (OK this is just an example of my first point).

Hmmm...wish I could remember. There was something about the "two-fold benefit of sex" but I can't remember what it was...

On the origins of sex (I almost wrote species :p ): I remember learning about the origin of mating types (i.e. eggs and sperm). So imagine we're starting off with early sex which involves two same-type sex cells (gametes) fusing. There is not male or female, or anything. Now suppose that through natural variation some of the individuals of the species that produce these produce smaller ones and others produce bigger ones. Those who produce smaller ones invest fewer resources in each, so can produce more; whilst those who produce bigger ones must produce fewer. There are therefore more small gametes than big gametes. At the moment they can fuse with any other type, but one can imagine that the most selectively advantageous strategy from the producer of the small gamete's point of view (if the fusion can be controlled) is for the smaller gamete to fuse with a large gamete as the larger gamete has more material resources within it with which to support the embryo subsequently produced. I can't remember how to work through the rest of this thought experiment, but I just thought I'd feed it into the discussion.

Really should dig out last year's notes when I'm back at Uni...Sorry for those disparate bits of information, hope they are of some relevance to the conversation. :)

Wed, 11 Jan 2012 22:04:17 UTC | #907514

Go to: Stupid and clever questions for people who understand the biology

JJFinch's Avatar Jump to comment 34 by JJFinch

          [Alan4discussion]

How do plants multiply up the number of their chromosomes in producing polyploid forms (eg tetraploid offspring) and how do hexaploid versions of triploid hybrids produce instant new species?

This happens through errors in meiosis in the gamete forming cells. Imagine two ordinary diploid parent plants. In their reproductive "bits" their cells undergo meiosis, whereby their paired chromosomes are (ultimately) unpaired and randomly packaged to form haploid gametes (i.e. cells with a single set of chromosomes, not two). Now, if, in the cells of one of these parents, an error occurs during meiosis such that the chromosome pairs do not separate, they may produce, instead of two haploid cells, a diploid cell and one with no chromosomes (which is not viable and will perish). If this diploid gamete meets up during a fertilisation event with an ordinary haploid gamete a triploid plant will be formed. The multiplication of the plant's chromosomes happens at this early stage. Triploid plants, whilst able to survive are usually infertile due to the odd number of chromosomes disrupting meiosis . Very rarely however, complete non-disjunction of the chromosomes may occur at meiosis such that a triploid gamete is produced, which, when fertilised with a haploid gamete produce a tetraploid plant. Tetraploids (or indeed any even number polyploid) can usually undergo meiosis without issue - it is the odd number polyploids that are usually infertile. Worth noting that it is not necessary for a triploid to have been formed and be viable for a tetraploid to form as a tetraploid can also result from the joining of two diploid gametes, which are not that rare.

To answer the second part of your question (which, I imagine, refers to wheat?), it's quite simple: doubling the genome size, via a hybridisation event (the meiotic errors described above occur more frequently in first generation hybrids due to slight mismatching of chromosomes) firstly introduces a heck of a lot of new variation into each of the parent gene pools. It is instantly selectively different, phenotypically different and to a certain extent reproductively isolated (though back-crossing to the parent species often can occur). Moreover, having doubles of chromosomes that are likely to contain many of the same genes opens up a veritable Smorgasboard of new functions to be acquired and rapidly selected by natural selection. Just as intra-chromosomal gene duplication can give rise to different genes in teh same family, entire genome duplication can allow genes to mutate without endangering the plant and to subsequently acquire new functions. This can lead to very rapid speciating selection. I hope that answers your question? :)

Fri, 06 Jan 2012 21:43:22 UTC | #906071

Go to: Stupid and clever questions for people who understand the biology

JJFinch's Avatar Jump to comment 33 by JJFinch

           [The Jersey Devil]

                 2)  Interesting.  I can even imagine the possibility that some mutations do not have a selection bias and could still infiltrate a population.  For example, I would not be surprised if eye color in humans has a neutral selection bias which is why we have a population with green eyes, brown eyes, blue eyes, etc.  Of course, in the long run we need a non-random process like natural selection to achieve anything interesting but I suspect a fair amount of ‘drift’ is possible.>

You are correct to imagine that some mutations and (not as often) the new phenotypes they produce may be neutral. This can happen for a number of reasons: as the genetic code is a degenerate code (that is, a given amino acid building block of a protein can be encoded by several different codons, triplets of three DNA bases) a single base pair substitution may not cause a change in the amino acid code of the protein produced. Or, a mutation may result in the replacement of one amino acid with another that has more or less the same properties as the one it is replacing (e.g. negatively charged) so that the protein is not affected (to the point of its function being changed). Where it gets more interesting is the level at which you are talking in which a different phenotype is produced but is still selectively neutral. Some would argue that this rarely, if ever, is the case though - what you must remember is that there are many different mechanisms by which stable polymorphisms (that is, phenotypic variation that exists in a population and is not transient, e.g. your eye-colour example) can arise; it does not depend on the traits being equal in selective terms.

My favourite of these mechanisms is heterozygote advantage (also known as the Wallace Effect) whereby variation at a single biallelic locus is maintained due to the heterozygous form being selectively favoured over either of the homozygous forms. The usual example given of this is sickle cell disease. This is a recessive disease (meaning to be a sufferer you must have two copies, be homozygous, for the faulty gene) and the diseased state is certainly worse than the dominant healthy state. So why does sickle-cell still exist? The clue is that it is prevalent in areas where Malaria, too, is prevalent, and the reason is that people who are carriers of the faulty gene (i.e. have one copy, are heterozygous) do not suffer from the disease and in addition are tolerant to malaria, so are at a selective advantage over both homozygote forms. This maintains the sickle cell gene in the population. Another example (because that last one has been done to death) is Cystic Fibrosis, another recessive disease. This has a carrier frequency of around 1 in 25 Caucasians (depending on where you are), but is almost absent in most other racial groups. It has been suggested that the heterozygotes (who do not suffer from CF and are healthy) may be resistant to TB and Cholera, which were both huge selective pressures on Caucasian populations in the past. As long as the genes for these diseases exist in a population the diseased phenotype can be produced, even though it is massively deleterious (in both these conditions, especially under natural conditions, pre-medicine).

Another group of mechanisms which can maintain morphological variation is frequency-dependent selection. This means that the selective value of a particular trait varies according to its frequency in the population. Negative frequency-dependent selection means that a trait is most advantagous when it is rare, subsequently increases in frequency (while the common competing trait decreases in frequency), becomes common (while the other becomes rare) and the tables turn, maintaining an oscillation in the frequencies of the alleles, with neither ever reaching 100% nor 0% frequency in the population. For example, many predators target their prey using "search image formation" whereby they become particularly good at searching for their prey based on what they usually look like. If an individual in the prey population varies in its appearance such that it does not fit the predator's search image it will be less likely to be targetted and will enjoy a selectivel advantage - that is, until its progeny bearing the same trait, have become sufficiently common for the predator to form a search image of them, such that they are the commonly targetted form. And so on, I'm sure you get the idea.

Oh and, of course, there is also as you said, simply genetic drift.

Thought you might be interested in this, The Jersey Devil, based on your comment, sorry for the essay! :P I just find it quite cool. :)

Fri, 06 Jan 2012 21:23:30 UTC | #906065

Go to: Richard Dawkins on Sky News, TODAY, 1.30pm GMT

JJFinch's Avatar Jump to comment 21 by JJFinch

Ah, I missed it - is a video available?

Sat, 17 Dec 2011 13:53:06 UTC | #900297

More Comments by JJFinch