Here is an article published by the Southern Regional Aquaculture Center on basic aquaculture genetics. I found it to be a great read and is a bit more than what most would call "basic".
http://www.thefishsite.com/articles/...lture-genetics
Here is an article published by the Southern Regional Aquaculture Center on basic aquaculture genetics. I found it to be a great read and is a bit more than what most would call "basic".
http://www.thefishsite.com/articles/...lture-genetics
Thanks Dan, looks like a winner.
Jon
He attacked everything in life with a mix of extraordinary genius and naive incompetence, and it was often difficult to tell which was which.
- Douglas Adams
http://www.mugwump-fish-world.com/index.php
Definitely a good read! I highly recommend this primer.
One thing I would add to this is a small expansion on what they refer to as additive effects, as this is something that directly affects angelfish breeding.
In most organisms that people breed for recreational purposes, the traits we focus on are generally related to colour or morphological features (such as V in angels) and these features and gene interactions are well known. Most people are also aware that for those genes that are known, there are many genes that are not known and the sum of an organism's phenotype is due to these known genes and the unknown ones (not taking into account the environment, for the sake of this reply). This is why we can look at some people and say they have blue eyes, and then look at other people and say they have REALLY blue eyes, because the other genetic (and environmental) factors influencing the expression of the blue-eyed phenotype have lined up in such a way as to accentuate the trait, while in other people their blue eyes are more grey than blue. However, despite the grey cast to their eyes they are still considered to be genetically blue-eyed.
When a gene's expression is influenced, or modified, by other genes we call it polygenetic and the unknown genes, or polygenes, can be small in number, or large. As technology and research improves and more genes and their functions are mapped, these interactions become more well known. Initially, however, these modifying genes are unknown to us. I worked out a little way of thinking about these modifying genes that has helped me enormously over the years breeding things from rabbits, to roses (you have no idea the different permutations of pink you can get in a rose ). Polygenes, like other genes, exist in pairs that are affected by different inheritance patterns, such as regular dominant and recessive patterns or other Mendelian and non-Mendelian interactions. We have a problem because we don't know what those genes are, but we can clearly see their effects. Through the magic of independent assortment and segregation an individual's genotype can contain varying combinations of polygenes that can either accentuate a trait or appear to reduce it. This is why these genes appear to be additive (or subtractive), but I find that people new to genetics often develop misconceptions around this because they come to the conclusion that by selective breeding they can continue to accumulate these polygenes that either accentuate or reduce a trait ad infinatum but that would mean that the organism's chromosomes would continue to fluctuate in length, as these polygenes were either added or subtracted from the total complement of genes on them... you can't just keep adding new loci to a chromosome. They were always there. We just don't know what they are!
I think of polygenes as either a + or a -. The more + polygenes the individual has, the more it affects the phenotypic expression of a trait. The more - polygenes they have the less pronounced the phenotypic expression will be. Just to re-emphasise a point I made earlier, that does not mean I can just keep accumulating + factors because there might only be two other genes affecting the expression of a trait, or twenty, but there is always a finite number of them and really they are like binary toggle switches which have either an on or and off state (or a dominant or recessive... or something else state) and once all those polygenes are accounted for you can reach a maximum or minimum phenotypic expression for that trait. To illustrate what I mean I'll use a simple, fictitious, example which describes how it works and also how to apply it to breeding programs.
Consider a trait A. A has simple dominant/recessive Mendelian inheritance but its expression is affected by two polygenes at different loci. An individual that is homozygous at the A locus, whose polygenes have maximal influence over A, would have the genotype A/A +/+ +/+, and a homozygous A individual whose polygenes had the minimum effect would be A/A -/- -/-. DOn't confuse the + for meaning wild type. I use the + to represent the additive nature of polygenes and because they are at different, unknown loci I treat them differently and separately to the genes we already have a good understanding of. So lets say an individual that had a full compliment of + modifiers that was A/A +/+ +/+ was crossed with an individual that had a full compliment of - modifiers that was A/A -/- -/-. The resulting progeny would be A/A +/- +/- and I would expect this individual to have an intermediate expression of the trait. If these individuals were inbred in an F1 cross, i.e. A/A +/- +/- x A/A +/- +/-, resulting in progeny that were either +/+ +/+, -/- -/-, +/+ -/-, +/-,+/- (or -/+ -/+), +/+ +/- (or -/+), or -/- +/- (or -/+). So you would expect to get a wide variation in the influence the polygenes had on A but because we can see the effect we can also select individuals that appear to have the highest compliment of + modifiers. This means we can line breed for an additive trait by selecting the ones with the largest or smallest expression or influence on A and then develop true-breeding lines for a degree of influence. It also means that if, after multiple generations, no more gains are being made in the level of expression we can assume that the modifiers are a full compliment of + type modifiers.
The kicker is, with don't know how many polygenes are influencing a particular trait so can't assign a particular number of + or - genes to them and would need to eliminate the environment as a causal agent, too.
You won't find any references to this kind of thinking, I don't think (I haven't looked), as it is just something I have been playing around with over the years to help me deal with the plethora of unknown genes in breeding programs that influence the expression of genes that we do know and it seems to work. I don't have any testing or references to back it up. The thing to watch is that this is different to multiple loci traits whose expression is dependent on more than one genes being present, if it is to be expressed at all, and one of the challenges is to distinguish between a trait that is additive and one that is caused by some other mode of inheritance. Wifi is one such trait that might cause confusion. You guys have said that line-breeding doesn't seem to affect the appearance or expression of wide-fins as they seem to turn up randomly and have a random degree of expression which suggests some other mode of inheritance. A trait that might be additive might be something like the level of blue in pb/pb individuals and that blue can be selected for and intensified by choosing the most blue individuals for breeding.
Hope this makes sense...
Last edited by TasV; 07-31-2015 at 07:48 PM.
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