Zwirko

Study the pedigree and write down your observations. My attempt notes three pertinent facts: 1. Higher prevalence of affected females. 2. All daughters of the affected father are affected AND none of his sons are affected. 3. The mother of an affected son is also affected. From there the answer should be obvious (I don't know the homework rules here, so I'll leave the final step up to you).

OMIM (Online Mendelian Inheritance in Man) might be a good resource. For example, on Rett syndrome, population genetics section it says:

Nobody knows for certain the exact details of what causes Turner syndrome, the so called molecular pathology remains elusive. There are, however, two general ideas. The first suggests that two active X-chromosomes are somehow required during very early development. Support for this comes from the observation that X-inactivation does not happen immediately upon fertilisation, but rather seems to occurs a few days later during the blastocyst stage. A more popular idea makes use of the observation that not all genes on the inactivated X are actually inactive - perhaps something like 25% escape inactivation at some stage, with about 15% completely escaping inactivation. Loss of an X chromosome can thus result in a haploinsufficiency - insufficient gene dosage - when a required active gene on the otherwise inactive X is lost; such a gene or genes are likely to have counterparts on the male Y-chromosome. In addition, genes can also randomly escape inactivation leading to too much of a particular gene product.

Most operons - including the E. coli lac and trp operons - in bacteria are regulated negatively through the action of repressor proteins; this can be achieved through both induction and repression. So a repressor protein can either keep a gene inactive or switch it off if it's active - both occur through the action of a repressor, hence these systems are characterised as being negatively regulated. The lac operon is an example of an inducible operon - a ligand inactivates the repressor and induces gene expression. The trp operom is an example of a repressible operon - a ligand activates the repressor and represses gene expression.

How does your entropy-information issue deal with the recent work with laboratory-evolved RNA enzymes? And their ability to rapidily evolve within hours? There are even "molecular speciation" experiments with competing ribozymes exploring new niches and adapting to their environments. Lots of mutations and new function evolving rapidly within a single day. Specifically, I'm referring to the continuous in vitro evolution/serial transfer/micro-fluidics experiments of Gerald Joyce and others.