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MAP Kinase-Mediated Negative Regulation of Symbiotic Nodule Formation in Medicago truncatula
Ryu, Hojin,Laffont, Carole,Frugier, Florian,Hwang, Ildoo Korean Society for Molecular and Cellular Biology 2017 Molecules and cells Vol.40 No.1
Mitogen-activated protein kinase (MAPK) signaling cascades play critical roles in various cellular events in plants, including stress responses, innate immunity, hormone signaling, and cell specificity. MAPK-mediated stress signaling is also known to negatively regulate nitrogen-fixing symbiotic interactions, but the molecular mechanism of the MAPK signaling cascades underlying the symbiotic nodule development remains largely unknown. We show that the MtMKK5-MtMPK3/6 signaling module negatively regulates the early symbiotic nodule formation, probably upstream of ERN1 (ERF Required for Nodulation 1) and NSP1 (Nod factor Signaling Pathway 1) in Medicago truncatula. The overexpression of MtMKK5 stimulated stress and defense signaling pathways but also reduced nodule formation in M. truncatula roots. Conversely, a MAPK specific inhibitor, U0126, enhanced nodule formation and the expression of an early nodulation marker gene, MtNIN. We found that MtMKK5 directly activates MtMPK3/6 by phosphorylating the TEY motif within the activation loop and that the MtMPK3/6 proteins physically interact with the early nodulation-related transcription factors ERN1 and NSP1. These data suggest that the stress signaling-mediated MtMKK5/MtMPK3/6 module suppresses symbiotic nodule development via the action of early nodulation transcription factors.
MAP Kinase-Mediated Negative Regulation of Symbiotic Nodule Formation in Medicago truncatula
류호진,Carole Laffont,Florian Frugier,황일두 한국분자세포생물학회 2017 Molecules and cells Vol.40 No.1
Mitogen-activated protein kinase (MAPK) signaling cascades play critical roles in various cellular events in plants, including stress responses, innate immunity, hormone signaling, and cell specificity. MAPK-mediated stress signaling is also known to negatively regulate nitrogen-fixing symbiotic interactions, but the molecular mechanism of the MAPK signaling cas-cades underlying the symbiotic nodule development remains largely unknown. We show that the MtMKK5-MtMPK3/6 signaling module negatively regulates the early symbiotic nodule formation, probably upstream of ERN1 (ERF Required for Nodulation 1) and NSP1 (Nod factor Signaling Pathway 1) in Medicago truncatula. The overexpression of MtMKK5 stimulated stress and defense signaling pathways but also reduced nodule formation in M. truncatula roots. Conversely, a MAPK specific inhibitor, U0126, enhanced nodule formation and the expression of an early nodulation marker gene, MtNIN. We found that MtMKK5 directly activates MtMPK3/6 by phosphorylating the TEY motif within the activation loop and that the MtMPK3/6 proteins physically interact with the early nodulation-related transcription factors ERN1 and NSP1. These data suggest that the stress signaling-mediated MtMKK5/MtMPK3/6 module sup-presses symbiotic nodule development via the action of early nodulation transcription factors.
Strategic Cross-Subsidies and Vertical Integration in Opening Telecommunications Markets
F. Gasmi,J. J. Laffont,W. W. Sharkey 서울대학교 경제연구소 2001 Seoul journal of economics Vol.14 No.3
This paper analyzes the strategic role of cross-subsidies under vertical integration. We consider an incumbent firm which operates in a regulated market (switched telecommunications service) and a competitive market (unswitched service). Fitting cost data generated with an engineering cost proxy model to smooth functional forms, we first assess the extent of cross-subsidies due to allocation of common costs and managerial effort. We then focus on the cost incentives of the regulatory scheme in the regulated segment and identify situations where the incumbent may blockade entry in the competitive segment.