Structural gene

A structural gene is a gene that codes for any RNA or protein product other than a regulatory factor (i.e. regulatory protein). A term derived from the lac operon, structural genes are typically viewed as those containing sequences of DNA corresponding to the amino acids of a protein that will be produced, as long as said protein does not function to regulate gene expression. Structural gene products include enzymes and structural proteins. Also encoded by structural genes are non-coding RNAs, such as rRNAs and tRNAs (but excluding any regulatory miRNAs and siRNAs). A structural gene is a gene that codes for any RNA or protein product other than a regulatory factor (i.e. regulatory protein). A term derived from the lac operon, structural genes are typically viewed as those containing sequences of DNA corresponding to the amino acids of a protein that will be produced, as long as said protein does not function to regulate gene expression. Structural gene products include enzymes and structural proteins. Also encoded by structural genes are non-coding RNAs, such as rRNAs and tRNAs (but excluding any regulatory miRNAs and siRNAs). In prokaryotes, structural genes of related function are typically adjacent to one another on a single strand of DNA, forming an operon. This permits simpler regulation of gene expression, as a single regulatory factor can affect transcription of all associated genes. This is best illustrated by the well-studied lac operon, in which three structural genes (lacZ, lacY, and lacA) are all regulated by a single promoter and a single operator. Prokaryotic structural genes are transcribed into a polycistronic mRNA and subsequently translated. In eukaryotes, structural genes are not sequentially placed. Each gene is instead composed of coding exons and interspersed non-coding introns. Regulatory sequences are typically found in non-coding regions upstream and downstream from the gene. Structural gene mRNAs must be spliced prior to translation to remove intronic sequences. This in turn lends itself to the eukaryotic phenomenon of alternative splicing, in which a single mRNA from a single structural gene can produce several different proteins based on which exons are included. Despite the complexity of this process, it is estimated that up to 94% of human genes are spliced in some way. Furthermore, different splicing patterns occur in difference tissue types. An exception to this layout in eukaryotes are genes for histone proteins, which lack introns entirely. Also distinct are the rDNA clusters of structural genes, in which 28S, 5.8S, and 18S sequences are adjacent, separated by short internally transcribed spacers, and likewise the 45S rDNA occurs five distinct places on the genome, but is clustered into adjacent repeats. In eubacteria these genes are organized into operons. However, in archaebacteria these genes are non-adjacent and exhibit no linkage. The identification of the genetic basis for the causative agent of a disease can be an important component of understanding its effects and spread. Location and content of structural genes can elucidate the evolution of virulence, as well as provide necessary information for treatment. Likewise understanding the specific changes in structural gene sequences underlying a gain or loss of virulence aids in understanding the mechanism by which diseases affect their hosts. For example, Yersinia pestis (the bubonic plague) was found to carry several virulence and inflammation-related structural genes on plasmids. Likewise, the structural gene responsible for tetanus was determined to be carried on a plasmid as well. Diphtheria is caused by a bacterium, but only after that bacterium has been infected by a bacteriophage carrying the structural genes for the toxin. In Herpes simplex virus, the structural gene sequence responsible for virulence was found in two locations in the genome despite only one location actually producing the viral gene product. This was hypothesized to serve as a potential mechanism for strains to regain virulence if lost through mutation. Understanding the specific changes in structural genes underlying a gain or loss of virulence is a necessary step in the formation of specific treatments, as well the study of possible medicinal uses of toxins. As far back as 1974, DNA sequence similarity was recognized as a valuable tool for determining relationships among taxa. Structural genes in general are more highly conserved due to functional constraint, and so can prove useful in examinations of more disparate taxa. Original analyses enriched samples for structural genes via hybridization to mRNA.