ppGpp directly inhibits transcription from ribosomal promoters.  One model is ppGpp and DksA together and independently decrease the stability of the open complexes formed on DNA by RNAP.  Another model is the trapping mechanism. In this model, RNAP is trapped by ppGpp in closed complexes and is unable to initiate transcription. Thus, ppGpp seems to act at many levels, and the mechanism of its action is a complex outcome of several factors, intrinsic promoter properties not being the least of them. The transcription activation by ppGpp can be direct or indirect. Direct activation occurs when RNAP interacts with effectors, such as ppGpp, DksA or both, to increase transcription from a given promoter. Indirect activation by these effectors of one promoter relies on inhibition of other (strong) promoters, leading to increased availability of RNAP that indirectly activates transcription initiation. The promoters that activated directly by ppGpp include PargI, PthrABC, PlivJ, and PhisG. The indirectly activation promoters include these dependent on sigma factors: S, H, N, E. When strong promoters, such as rrn, are inhibited, there more RNAP are available for these alternative sigma factors.