Trp operon genes are arranged in the same order in E. coli and Bacillus subtilis. [1]The arrangement of the trp operon in E. coli and Bacillus subtilis differs. There are 5 structural genes in E. colithat are found under a single transcriptional unit. InBacillus subtilis, there are 6 structural genes that are situated within a supraoperon. Three of these genes are found upstream while the other three genes are found downstream of the trp operon.[2]There is a 7th gene inBacillus subtilis's operon called trpG or pabA which is responsible for protein synthesis of tryptophan and folate.[3] Regulation of trp operons in both organisms depends on the amount of trp present in the cell. However, the primary regulation of tryptophan biosynthesis in B. subtilis is via attenuation, rather than repression, of transcription.[4] In B. subtilis, tryptophan binds to the eleven-subunit tryptophan-activated RNA-binding attenuation protein (TRAP), which activates TRAP's ability to bind to the trp leader RNA.[5][6] Binding of trp-activated TRAP to leader RNA results in the formation of a terminator structure that causes transcription termination.[4]In addition, the activated TRAP inhibits the initiation of translation of trpP, trpE, trpG and ycbK genes. The gene trpP plays a role in trp transportation, while the gene trpG is utilized in the folate operon, and the gene ycbK is involved in synthesis of an efflux protein. The activated TRAP protein is regulated by an anti-TRAP protein and AT synthesis. AT can inactive TRAP to lower the transcription of tryptophan.[7]
^Yanofsky, Charles (2004). The different roles of tryptophan transfer RNA in regulating trp operon expression in E. coli versus B. subtilis (20 ed.). Department of Biological Sciences, Stanford University, Stanford, CA 94305, USA: Oxford: Elsevier Ltd. pp. 367–369. doi:10.1016/j.tig.2004.06.007.{{cite book}}: CS1 maint: location (link)
^ abGollnick P, Babitzke P, Antson A, Yanofsky C (2005-11-14). "Complexity in regulation of tryptophan biosynthesis in Bacillus subtilis". Annual Review of Genetics. 39 (1): 47–68. doi:10.1146/annurev.genet.39.073003.093745. PMID16285852.
