Hereditary profiles of disorderly transcription?

Background  

Microscopic examination of living cells often reveals that cells from some cell strains appear to be in a permanent state of disarray without obvious reason. In all probability such a disorderly state affects cell functioning.     

Iron homeostasis in plants： when transcription affects translocation

Despite the fact that iron is one of the most abundant elements of the earth＇s crust, iron deficiencies are serious problems both in human nutrition [ 1 ] and in agriculture [2]. Six to eight percent of the world＇s population is potentially affected by iron deficiency induced anemia, a leading cause of maternal death in African and Asian countries where people rely mostly on plants for their daily intake of iron. Iron can also be a limiting factor in the growth of economically important crop plants because of inadequate soil chemistry, and such deficiencies cannot easily be corrected by amending the soil. Improving the plant＇s ability to absorb iron in adverse conditions and to increase their overall content could offer solutions to these dramatic problems. Therefore understanding the molecular mechanisms regulating iron uptake and homeostasis in plants has potentially important practical applications both in agriculture and human health [3].     

Blockers and barriers to transcription: competing activities?

In the eukaryotic cell active and inactive genes reside adjacent to one another and are modulated by numerous regulatory elements. Insulator elements prevent the misregulation of adjacent genes by restricting the effects of the regulatory elements to specific domains. Enhancer blockers prevent enhancers from inadvertently activating neighboring genes, and recent results suggest that they might function by a conserved mechanism across species. These elements appear to disrupt enhancer-promoter "communications" by interacting with the regulatory elements and sequestering these elements into specific regions of the nucleus thus rendering them non-functional. Barrier elements insulate active genes from neighboring heterochromatin and recent results suggest that they function by specific localized recruitment of acetyltransferases that antagonize the spread of heterochromatin-associated deacetylases, thus preventing the propagation of heterochromatin.