Dominant genes always need to suppress the recessive genes in a definite way.But which type of regulation they prefer? Transcriptional? Translational?
If transcriptional then does the LCR do the job, or miRNA supression or histone relocalization or deacetalysation of histones cause this?
To my knowledge, dominant *alleles* (dominance relationships hold between alleles of the same gene, not between different genes) do not "need" to suppress anything. Different alleles simply *happen* to give rise to dominance hierarchies in the phenotype.
For example, in the most basic case, a functional allele does not "need" anything to be dominant on a non-functional allele: the functional allele expresses the protein, and as such it is dominant; you need two non-functional copies to get a phenotype coming from the absence of the protein.
I would start very simply from here: http://en.wikipedia.org/wiki/Dominance_%28genetics%29 to understand how dominance works.
( There are much more complex cases of course, including chromosome silencing or genomic imprinting, that is the differential expression of paternally inherited vs maternally inherited genes; in such cases there are active mechanisms into play).
Massimo is right. Most recessive traits are loss-of-function mutations. Therefore a normal allele will be dominant in this case because it can compensate for the defective protein encoded by the recessive allele. Dominant traits can also reflect gain-of-function mutations, in which any amount of the normal allele will be overwhelmed by the effect of unregulated or abnormal activity in the dominant allele.
Again, the key is that the phenotype is determined by the level of protein activity, and usually do not require any changes in chromatin state or gene expression.
thanks.yes functional protein may have a role in a particular pathway but do all recessive genes code for non functional proteins?or the protein formed by the dominant gene is more capable to perform a pathway which results in wild phenotype?
is this a case like competitive inhibition of inactive proteins by active protein.which may b regulated by promoter sequence.I.e which ever be highly conserved sequence or close to consensus sequence will transcriptionally more active and will produce more functional protein.again why we will not consider the combinatorial control of gene regulation.that may be one of the two allele has different transcription factor binding site .which will have all the possible combination will be active for a pathway.
-- "do all recessive genes code for non functional proteins?" --
Not necessarily. It is just a common (and trivial) scenario.
--"or the protein formed by the dominant gene is more capable to perform a pathway which results in wild phenotype?"--
This is a bit confused wording, but I guess the answer is "it is possible".
The rest of your post I can't understand, sorry - could you clarify? The shaky grammar makes it impossible to me to get what you mean.
Saswat- are you asking whether mutations in DNA regulatory sequence can impair gene expression and thus lead to a disease phenotype? If so, the answer is yes. Many disease-associated SNPs map to putative regulatory regions (promoters, intronic enhancers) and are thought to work by altering gene expression. However, these relationships between non-coding SNPs and disease are more often inferred than directly demonstrated.
The more commonly studied scenario whereby change in gene expression (as opposed to protein function) is linked to phenotype is genetic imprinting, such as maternal or paternally repressed genes.
The importance of hereditary changes in gene expression is a well-established phenomenon in genetics. They can be either epigenetic or genetic (such as the SNP example) in origin.
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