An EPFL peptide signaling pathway promotes stamen elongation via enhancing filament cell proliferation to ensure successful self-pollination in Arabidopsis thaliana.

Proper stamen filament elongation is essential for plant self-pollination and reproduction. Several phytohormones such as jasmonate and gibberellin play important roles in controlling filament elongation, but other endogenous signals involved in this developmental process remain unknown. We report here that three EPIDERMAL PATTERNING FACTOR-LIKE (EPFL) family peptides, EPFL4, EPFL5 and EPFL6, act redundantly to promote stamen filament elongation via enhancing filament cell proliferation in Arabidopsis thaliana. Knockout of EPFL4-6 genes led to shortened filaments due to defective filament cell proliferation, resulting in pollination failure and male sterility. Further genetic and biochemical analyses indicated that the ERECTA family and the SOMATIC EMBRYOGENESIS RECEPTOR KINASE (SERK) family RLKs form receptor complexes to perceive EPFL4-6 peptides and promote filament cell proliferation. Moreover, based on both loss- and gain-of-function genetic analyses, the mitogen-activated protein kinase cascade MKK4/MKK5-MPK6 was shown to function downstream of EPFL4-6 to positively regulate cell proliferation in stamen filaments. Together, this study reveals that an EPFL peptide signaling pathway composed of the EPFL4-6 peptide ligands, the ERECTA-SERK receptor complexes and the downstream MKK4/MKK5-MPK6 cascade promotes stamen filament elongation via enhancing filament cell proliferation to ensure successful self-pollination and normal fertility in Arabidopsis.

Overexpression of phzM contributes to much more production of pyocyanin converted from phenazine-1-carboxylic acid in the absence of RpoS in Pseudomonas aeruginosa.

Pyocyanin produced by Pseudomonas aeruginosa is a key virulence factor that often causes heavy damages to airway and lung in patients. Conversion of phenazine-1-carboxylic acid to pyocyanin involves an extrametabolic pathway that contains two enzymes encoded, respectively, by phzM and phzS. In this study, with construction of the rpoS-deficient mutant, we first found that although phenazine production increased, pyocyanin produced in the mutant YTΔrpoS was fourfold much higher than that in the wild-type strain YT. To investigate this issue, we constructed phzM-lacZ fusion on a vector and on the chromosome. By quantifying ß-galactosidase activities, we confirmed that expression of the phzM was up-regulated when the rpoS gene was inactivated. However, no changes occurred in the expression of phzS and phzH when the rpoS was knocked out. Taken together, overproduction of the SAM-dependent methyltransferase (PhzM) might contribute to the increased pyocyanin in the absence of RpoS in P. aeruginosa.