In Arabidopsis thaliana, multiple genes involved in shoot apical meristem (SAM) transitions have been characterized, but the mechanisms required for the dynamic attainment of vegetative, inflorescence, and floral meristem (VM, IM, FM) cell fates during SAM transitions are not well understood. Here we show that a MADS-box gene, XAANTAL2 (XAL2/AGL14), is necessary and sufficient to induce flowering, and its regulation is important in FM maintenance and determinacy. xal2 mutants are late flowering, particularly under short-day (SD) condition, while XAL2 overexpressing plants are early flowering, but their flowers have vegetative traits. Interestingly, inflorescences of the latter plants have higher expression levels of LFY, AP1, and TFL1 than wild-type plants. In addition we found that XAL2 is able to bind the TFL1 regulatory regions. On the other hand, the basipetal carpels of the 35S::XAL2 lines lose determinacy and maintain high levels of WUS expression under SD condition. To provide a mechanistic explanation for the complex roles of XAL2 in SAM transitions and the apparently paradoxical phenotypes of XAL2 and other MADS-box (SOC1, AGL24) overexpressors, we conducted dynamic gene regulatory network (GRN) and epigenetic landscape modeling. We uncovered a GRN module that underlies VM, IM, and FM gene configurations and transition patterns in wild-type plants as well as loss and gain of function lines characterized here and previously. Our approach thus provides a novel mechanistic framework for understanding the complex basis of SAM development.
SUMMARYPost-translational modification of proteins by attachment of small ubiquitin-like modifier (SUMO) is essential for plant growth and development. Mutations in the SUMO protease early in short days 4 (ESD4) cause hyperaccumulation of conjugates formed between SUMO and its substrates, and phenotypically are associated with extreme early flowering and impaired growth. We performed a suppressor mutagenesis screen of esd4 and identified a series of mutants called suppressor of esd4 (sed), which delay flowering, enhance growth and reduce hyperaccumulation of SUMO conjugates. Genetic mapping and genome sequencing indicated that one of these mutations (sed111) is in the gene salicylic acid induction-deficient 2 (SID2), which encodes ISOCHORISMATE SYNTHASE I, an enzyme required for biosynthesis of salicylic acid (SA). Analyses showed that compared with wild-type plants, esd4 contains higher levels of SID2 mRNA and about threefold more SA, whereas sed111 contains lower SA levels. Other sed mutants also contain lower SA levels but are not mutant for SID2, although most reduce SID2 mRNA levels. Therefore, higher SA levels contribute to the small size, early flowering and elevated SUMO conjugate levels of esd4. Our results support previous data indicating that SUMO homeostasis influences SA biosynthesis in wild-type plants, and also demonstrate that elevated levels of SA strongly increase the abundance of SUMO conjugates.
Ustilago maydis is a biotrophic pathogen and well-established genetic model to understand the molecular basis of biotrophic interactions. U. maydis suppresses plant defense and induces tumors on all aerial parts of its host plant maize. In a previous study we found that U. maydis induced leaf tumor formation builds on two major processes: the induction of hypertrophy in the mesophyll and the induction of cell division (hyperplasia) in the bundle sheath. In this study we analyzed the cell-type specific transcriptome of maize leaves 4 days post infection. This analysis allowed identification of key features underlying the hypertrophic and hyperplasic cell identities derived from mesophyll and bundle sheath cells, respectively. We examined the differentially expressed (DE) genes with particular focus on maize cell cycle genes and found that three A-type cyclins, one B-, D- and T-type are upregulated in the hyperplasic tumorous cells, in which the U. maydis effector protein See1 promotes cell division. Additionally, most of the proteins involved in the formation of the pre-replication complex (pre-RC, that assure that each daughter cell receives identic DNA copies), the transcription factors E2F and DPa as well as several D-type cyclins are deregulated in the hypertrophic cells.
34Ustilago maydis is a biotrophic pathogen and well-established genetic model to 35 understand the molecular basis of biotrophic interactions. U. maydis suppresses plant 36 defense and induces tumors on all aerial parts of its host plant maize. In a previous 37 study we found that U. maydis induced leaf tumor formation builds on two major 38 processes: the induction of hypertrophy in the mesophyll and the induction of cell 39 division (hyperplasia) in the bundle sheath. In this study we analyzed the cell-type 40 specific transcriptome of maize leaves 4 days post infection. This analysis allowed 41 identification of key features underlying the hypertrophic and hyperplasic cell identities 42 derived from mesophyll and bundle sheath cells, respectively. We examined the 43 differentially expressed (DE) genes with particular focus on maize cell cycle genes and 44found that three A-type cyclins, one B-, D-and T-type are upregulated in the 45 hyperplasic tumorous cells, in which the U. maydis effector protein See1 promotes cell 46 division. Additionally, most of the proteins involved in the formation of the pre-47replication complex (pre-RC, that assure that each daughter cell receives identic DNA 48 copies), the transcription factors E2Fand DPa as well as several D-type cyclins are 49 deregulated in the hypertrophic cells. 50 51Introduction 52 53Ustilago maydis is a biotrophic fungus that triggers tumors in all aerial parts of its host 54 plant maize (Zea mays). To attenuate activity of the maize immune system and colonize 55 the different maize organs, U. maydis deploys a set of proteins, so called effectors, 56which manipulate the plant cell metabolism, structure and function for its growth 57benefit. Such effectors are deployed in a time-, organ-and cell-type-specific manner to 58reprogram and/or cope with the different maize cell environments 1-11 . 59 60U. maydis infection induces characteristic symptoms that include chlorosis, which 61 appears 24 hours post infection (hpi), such lesions are produced in the absence of fungal 62 hyphae suggesting that they result from fungal products such as toxins or effectors 12 . 2 63 days post infection (dpi) anthocyanin streaking appears and fungal hyphae proliferate 64 and penetrate in between mesophyll cells. At 4 dpi the hyphae have reached the bundle 65 sheath cells and induce tumor formation while at 5 dpi small tumors are visible. 8 dpi 66 maize leaf cells are enlarged and fungal hyphae have undergone branching, a process 67 described as the beginning of teliospore formation 13,14 . Finally, at 12-14 dpi large 68 tumors are formed; inside such tumorous tissue hypha differentiate to give place to the 69 diploid teliospores 15 . Several studies have investigated maize transcriptional 70reprogramming in response to U. maydis infection 10,15-20 . On the cellular level, U. 71 maydis induced tumors in maize leaves were found to be constituted of hypertrophic 72 tumor (HTT) cells coming from transformed mesophyll cells (M), and hyperplasic 73 tumor (HPT) cells derived from b...
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