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- 저자 : Larrainzar, Estí (검색결과 2 건)
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Larrainzar, Estí,baliz,Riely, Brendan K.,Kim, Sang Cheol,Carrasquilla-Garcia, Noelia,Yu, Hee-Ju,Hwang, Hyun-Ju,Oh, Mijin,Kim, Goon Bo,Surendrarao, Anandkumar K.,Chasman, Deborah,Siahpirani, Alir American Society of Plant Biologists 2015 Plant Physiology Vol.169 No.1
<P><I>Transcriptional reprogramming is regulated by Nod factor-induced ethylene signaling.</I></P><P>The legume-rhizobium symbiosis is initiated through the activation of the Nodulation (Nod) factor-signaling cascade, leading to a rapid reprogramming of host cell developmental pathways. In this work, we combine transcriptome sequencing with molecular genetics and network analysis to quantify and categorize the transcriptional changes occurring in roots of <I>Medicago truncatula</I> from minutes to days after inoculation with <I>Sinorhizobium medicae</I>. To identify the nature of the inductive and regulatory cues, we employed mutants with absent or decreased Nod factor sensitivities (i.e. <I>Nodulation factor perception</I> and <I>Lysine motif domain-containing receptor-like kinase3</I>, respectively) and an ethylene (ET)-insensitive, Nod factor-hypersensitive mutant (<I>sickle</I>). This unique data set encompasses nine time points, allowing observation of the symbiotic regulation of diverse biological processes with high temporal resolution. Among the many outputs of the study is the early Nod factor-induced, ET-regulated expression of ET signaling and biosynthesis genes. Coupled with the observation of massive transcriptional derepression in the ET-insensitive background, these results suggest that Nod factor signaling activates ET production to attenuate its own signal. Promoter:β-glucuronidase fusions report ET biosynthesis both in root hairs responding to rhizobium as well as in meristematic tissue during nodule organogenesis and growth, indicating that ET signaling functions at multiple developmental stages during symbiosis. In addition, we identified thousands of novel candidate genes undergoing Nod factor-dependent, ET-regulated expression. We leveraged the power of this large data set to model Nod factor- and ET-regulated signaling networks using MERLIN, a regulatory network inference algorithm. These analyses predict key nodes regulating the biological process impacted by Nod factor perception. We have made these results available to the research community through a searchable online resource.</P>
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The CCAAT box-binding transcription factor NF-YA1 controls rhizobial infection
Laporte, Philippe,Lepage, Agnes,Fournier, Joë,lle,Catrice, Olivier,Moreau, Sandra,Jardinaud, Marie-Franç,oise,Mun, Jeong-Hwan,Larrainzar, Estibaliz,Cook, Douglas R.,Gamas, Pascal,Niebel, And Oxford University Press 2014 Journal of experimental botany Vol.65 No.2
<P>Symbiosis between legume plants and soil rhizobia culminates in the formation of a novel root organ, the ‘nodule’, containing bacteria differentiated as facultative nitrogen-fixing organelles. MtNF-YA1 is a <I>Medicago truncatula</I> CCAAT box-binding transcription factor (TF), formerly called HAP2-1, highly expressed in mature nodules and required for nodule meristem function and persistence. Here a role for MtNF-YA1 during early nodule development is demonstrated. Detailed expression analysis based on RNA sequencing, quantitiative real-time PCR (qRT-PCR), as well as promoter–β-glucuronidase (GUS) fusions reveal that <I>MtNF-YA1</I> is first induced at the onset of symbiotic development during preparation for, and initiation and progression of, symbiotic infection. Moreover, using a new knock-out mutant, <I>Mtnf-ya1-1</I>, it is shown that <I>MtNF-YA1</I> controls infection thread (IT) progression from initial root infection through colonization of nodule tissues. Extensive confocal and electronic microscopic observations suggest that the bulbous and erratic IT growth phenotypes observed in <I>Mtnf-ya1-1</I> could be a consequence of the fact that walls of ITs in this mutant are thinner and less coherent than in the wild type. It is proposed that <I>MtNF-YA1</I> controls rhizobial infection progression by regulating the formation and the wall of ITs.</P>
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