Explanation about the concepts of co-dominanace and incomplete dominance

[Frigus]

We were told that
incomplete dominance occurs when in heterozygous condition one of the allele is less efficient and another is normal/wild type/unmodified.
Co-dominanace occurs when in heterozygous condition both the alleles produce normal functioning enzyme but both the alleles produces different type of phenotype when are present in their respective homozygous condition.
Incomplete dominance is when the heterozygous condition of two alleles don't resembles to either of the homozygous parents and
co-dominanace is when heterozygous condition resembles both the homozygous parents.
So now problem is that we say incomplete dominance is when one of the allele produces less efficient enzyme but if we take case of MN blood group then even if one of the allele produces less efficient enzyme then the heterozygous progeny should resemble both the parents as one antigen is present in less amount and one in more.
Thanks.

 

[epenguin]

Put it this way: concept of 'more or less efficient enzyme' is not appropriate for the case you are considering of MN blood groups.

Put another way, there are genes, DNA sequences, and there is chain of consequences by which these become expressed as a protein and then a further consequences through which this results in a function or phenotype, all of which is molecular biology, biochemistry and other serious sciences. Genetics is molecular biology etc. by cheating I.e. what it was possible to do without knowing the chain of interactions in cases of a simple relationship gene variation/function I.e. phenotype in cases where this was easily observable by e.g. organism colour, nutritional dependence or - this case - an easy immunological test. To a first approximation there is no great survival value difference in the different common alleles in question here (otherwise they would not be so common).

A lot later than the discovery of this immunologically detectable variation, the hardworking biochemists etc. have found responsible for it is a transmembrane protein glycophorin A in the red blood cell which exists in two different common versions M and N. The part of the protein outside the cell gets polyglycosylated, well, or rather it is polyglycosylated (glycosyltransferase-catalysed) in the endoplasmic reticulum then transported to the cell surface and the polysaccharide part is outside the cell. It is the polysaccharide that it is the antigen. The M and N aminoacid sequences differ in two positions. This can cause differences in the protein confirmation which causes them to be glycosylated in different ways. (A grosser difference might be that M contains an N-terminal Ser which could be and apparently is O-glycosylated but N contains in this position Leu which cannot - https://www.biology-pages.info/G/Glycoproteins.html however in as much searching as I could, I found no one saying this apparently straightforward connection explicitly, so wonder if I've got this right.)

The polysaccharides attached to the Glycophorin A are very hydrophilic. This is said to have to do with the ease the cells pass in blood vessels. In fact the polysaccharide covers a large part of the blood cell surface so on both counts we see there might be many interactions whereby different Glycophorins might have sone biological/medical significance and so selective value in second approximation

 

[BillTre]

Genetics is molecular biology etc. by cheating I.e. what it was possible to do without knowing the chain of interactions in cases of a simple relationship gene variation/function I.e. phenotype

I agree the relationship between genes and their phenotypes is not always direct.

There is a difference between what I would call productive genetics (making organisms with particular traits through breeding techniques; which I take as your point) and investigative genetics (research).

In the history of research into genetics, things started out by scoring crosses (counting the numebr of different phenotypes in the progeny of a cross) based upon very easy to observe traits (like color, coat length, obvious behaviors). By observing inheritance patterns, inherited "factors" were tracked and were the first identified genes.
As more subtle traits were made useful in this approach, more genes (genetic locations) were identified, mapped (and afterward used for production).

Until the modern age of biology (resulting from understandings of how processes associated with the uniqueness of living things (DNA, RNA, proteins, etc.)) most (all?) genes were not really attached to any mechanism for generating their phenotypes. Genes were abstract, predictive mathematical concepts similar to how astronomers predicted the location of later discovered planets, like Pluto (well, non-planet now, I guess).

The modern biological understanding has shown the generative mechanisms of many phenotypes (as @epenguin has just shown) can be very complex. Many traits are now know to be affected by large numbers of genes to a very small extent, and are only detected in statistical surveys.

It is now possible to looked for mutations in organisms based upon traits of their DNA sequence, by using new screening techniques (easily repeatable, sensitive molecular tests) or selections (only those with/without particular sequences will survive/breed).
In a sense, any scoreable trait can indicate the presence of a gene (in the original use in genetics sense).
If it can be scored efficiently, it can be mapped and therefore identified a molecular sequence.

Because of the centrality of the explanations of molecular biology to our understanding of biology, all genes are often expected to be proteins encoded in DNA (or RNA in some organisms).
Not always so. There are lots of other interesting ways a non-coding section of DNA can have understandable molecular effects that can generate a score-able phenotype.
In addition, (as @epenguin has shown), phenotypes are not always produced by simple direct mechanisms.

My answer to the OP is that I have always had trouble with these kinds of categories. There are always cases in the complex molecular system that living things that will defy these simple classification systems.
On the other hand, examples like these get used in courses because involve common easily detectable in tests and are representative of important processes (like genes producing proteins having an effect).

My advise would be to learn the examples the cite. They will represent important mechanisms, but be aware there are exceptions involving more intricate relationships, that you will probably get to in higher level genetics or cell biology classes (guessing this is related to something in a class).