Two human-specific Neisserial pathogens, Neisseria gonorrhoeae and Neisseria meningitidis require the expression of type IV pili (tfp) for the initial attachment to the host during infection. However the mechanisms controlling the assembly and functionality of tfp are poorly understood. It is known that the gonococcal pilE gene, encoding the major subunit, is positively regulated by IHF, a multi-functional DNA binding protein. A Neisserial specific repetitive DNA sequence, termed the Correia Repeat Enclosed Element (CREE) is situated upstream of three pil loci; pilH/I/J/K/X, pilG/D and pilF. CREE have been shown to contain strong promoters and some CREE variants contain a functional IHF binding site. CREE might therefore be involved in the regulation of tfp biogenesis in pathogenic Neisseria. Site-directed and deletion mutagenesis on promoter::cat reporter constructs demonstrated that transcription of pilH-X and pilG/D is from a sigma(70) promoter, and is independent of CREE. The insertion of CREE in the pilF promoter region in N. meningitidis generated a functional sigma(70) promoter. However there is also a functional promoter at this position in N. gonorrhoeae where there is no CREE. These results suggest CREE insertion in these three pil loci does not influence transcription and that IHF does not appear to co-ordinately regulate tfp biogenesis.