3.10 Inheritance, Environment and Expression

During formation of gametes and early embryonic development, extensive epigenetic reprogramming removes many marks and establishes new patterns. This reset limits transmission of acquired chromatin states. Some loci are exceptions. In genomic imprinting, expression depends on whether an allele came from the mother or father because one parental copy carries a silencing mark.

Imprinting means that two alleles with the same DNA sequence can have different activity according to parental origin. It also makes a locus vulnerable because only one copy may be active. Deletion or disruption of a chromosome region can therefore produce different syndromes depending on which parent's active contribution is lost. The inheritance remains based on DNA and gametes, but expression does not follow the simplest assumption that both alleles contribute equally.

Animal studies, including the agouti mouse model, show that maternal nutritional conditions can be associated with methylation differences and offspring phenotype. Such results demonstrate biological plausibility for environment-sensitive marks. They do not justify assuming that any acquired human characteristic passes epigenetically to grandchildren. Transgenerational claims require careful separation of direct exposure, shared environment, genetic variation and persistent germ-line marks.

Monozygotic twins originate from one zygote and begin with extremely similar genomes. Differences that develop in methylation, expression, disease or other phenotypes can therefore help reveal non-sequence influences. Age, different exposures and random cellular events may produce epigenetic divergence. Twins are powerful matched comparisons, but they do not isolate one environmental variable automatically and are not perfectly identical in every mutation or developmental condition.

Pollutants including particulate matter and some metals or organic chemicals are associated with altered methylation and inflammatory pathways. A credible mechanism requires evidence connecting exposure to a mark, the mark to altered expression and the expression change to phenotype. Epidemiological associations may be affected by diet, socioeconomic conditions, other exposures and disease itself. Experimental and longitudinal evidence helps establish direction and causality.

Steroid hormones can cross the plasma membrane and bind intracellular receptors. The hormone–receptor complex acts directly or indirectly as a transcription regulator at specific response elements, changing expression of target genes. Other hormones bind membrane receptors and activate signalling cascades that modify transcription factors. A hormone affects only cells with the required receptor and response machinery.

The E. coli lac operon coordinates genes needed for lactose use. Without lactose, a repressor binds the operator and blocks transcription. When lactose is available, an inducer derived from it reduces repressor binding. Expression is strongest when glucose is also scarce: low glucose favors an active CAP regulator that helps RNA polymerase bind. The operon integrates two environmental signals rather than acting as a simple lactose switch.

When glucose and lactose are both present, the repressor may be released but CAP stimulation remains low, so transcription is limited. With lactose present and glucose absent, repression is relieved and positive control is strong. This economy prevents bacteria from investing heavily in lactose-metabolizing enzymes while an easier carbon source is available. It is gene regulation by external nutrient conditions, not an epigenetic change inherited across bacterial generations.