Conserved motifs in a divergent nod box of Azorhizobium caulinodans ORS571 reveal a common structure in promoters regulated by LysR-type proteins.

Abstract

Nodulation of leguminous plants by Rhizobium, Bradyrhizobium, and Azorhizobium spp. is dependent on the induction by the plant host of different bacterial modulation (nod) loci. The transcription of these nod loci is activated in the presence of plant-produced flavonoids upon binding of the

Root-hair endophyte stacking in finger millet creates a physicochemical barrier to trap the fungal pathogen Fusarium graminearum

“…The Tn5 insertion localized to another member of the LysR transcriptional regulator family (ewfR), transcribed in the opposite direction as the ewf operon. The LysR canonical binding site sequence (TN 11 A) 29 was observed upstream of the ewfB-J coding sequences (Fig. 4h).…”

“…LysR was transcribed in the opposite direction as the operon. The LysR canonical binding site sequence (TN 11 A) 29 was observed upstream of the phzF (ewaF) coding sequences (Fig. 4b).…”

Functional Dissection of the LysR-type CysB Transcriptional Regulator

“…Most of the N-terminal residues identified in CysB as important for DNA binding are highly conserved among LTTRs. It was proposed (9) that highly conserved amino acids contact conserved base pairs of a generic TN 11 A motif present in the binding sites for most LTTRs (38). Some CysB residues (i.e.…”

The LysR-type PcaQ protein regulates expression of a protocatechuate-inducible ABC-type transport system in Sinorhizobium meliloti

“…To activate transcription, many LysR proteins have been demonstrated to require direct interaction with the C-terminal domain of the RNA polymerase (RNAP) alpha subunit (aCTD-RNAP) (Tao et al, 1993;Chugani et al, 1997;McFall et al, 1998;Fritsch et al, 2000;Park et al, 2002). In 1992, Goethals and co-workers identified a LysR DNA-binding motif (TN 11 A) present in the majority of binding sites (Goethals et al, 1992); however, the in silico prediction of LysR regulatory binding sequences is compromised by the prevalence of this motif within AT-rich intergenic regions.…”