SummaryPosttranslational acetylation of histones is reversibly regulated by histone deacetylases (HDACs). Despite the evident significance of HDACs in Arabidopsis development, the biological roles and underlying molecular mechanisms of many HDACs are yet to be elucidated.By a reverse-genetic approach, we isolated an hda9 mutant and performed phenotypic analyses on it. In order to address the role of HDA9 in flowering, genetic, molecular, and biochemical approaches were employed.hda9 flowered early under noninductive short-day (SD) conditions and had increased expression of the floral integrator FLOWERING LOCUS T (FT) and the floral activator AGAMOUS-LIKE 19 (AGL19) compared with the wild-type. The hda9 mutation increased histone acetylation and RNA polymerase II occupancy at AGL19 but not at FT during active transcription, and the HDA9 protein directly targeted AGL19. AGL19 expression was higher under SD than under inductive long-day (LD) conditions, and an AGL19 overexpression caused a strong up-regulation of FT. A genetic analysis showed that an agl19 mutation is epistatic to the hda9 mutation, masking both the early flowering and the increased FT expression of hda9.Taken together, our data indicate that HDA9 prevents precocious flowering under SD conditions by curbing the hyperactivation of AGL19, an upstream activator of FT, through resetting the local chromatin environment.

Plant immunity depends on massive expression of pathogenesis-related genes (PRs) whose transcription is de-repressed by pathogen-induced signals. Salicylic acid (SA) acts as a major signaling molecule in plant immunity and systemic acquired resistance triggered by bacterial or viral pathogens. SA signal results in the activation of the master immune regulator, Nonexpressor of pathogenesis-related genes 1 (NPR1), which is thought to be recruited by transcription factors such as TGAs to numerous downstream PRs. Despite its key role in SA-triggered immunity, the biochemical nature of the transcriptional coactivator function of NPR1 and the massive transcriptional reprogramming induced by it remain obscure. Here we demonstrate that the CBP/p300-family histone acetyltransferases, HACs and NPR1 are both essential to develop SA-triggered immunity and PR induction. Indeed HACs and NPR1 form a coactivator complex and are recruited to PR chromatin through TGAs upon SA signal, and finally the HAC-NPR1-TGA complex activates PR transcription by histone acetylation-mediated epigenetic reprogramming. Thus, our study reveals a molecular mechanism of NPR1-mediated transcriptional reprogramming and a key epigenetic aspect of the central immune system in plants.

Patient: Male, 49Final Diagnosis: T-lymphoid/myeloid bilineal blastic transformation of CMLSymptoms: Rapidly enlarging mass in left neckMedication: —Clinical Procedure: Biopsy of the left submandibular lymph nodesSpecialty: HematologyObjective:Rare co-existance of disease or pathologyBackground:Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder characterized by the Philadelphia chromosome generated by the reciprocal translocation t(9: 22)(q34;q11). CML is usually diagnosed in the chronic phase. Blast crisis represents an advanced phase of CML. Extramedullary blast crisis as the initial presentation of CML with bone marrow remaining in chronic phase is an unusual event. Further, extramedullary blast crisis with T lymphoid/myeloid bilineal phenotype as an initial presentation for CML is extremely unusual.Case Report:Here, we report the case of a 49-year-old male with rapidly enlarged submandibular lymph nodes. Biopsy specimen from the nodes revealed a characteristic appearance with morphologically and immunohistochemically distinct myeloblasts and T lymphoblasts co-localized in 2 adjacent regions, accompanied by chronic phase of the disease in bone marrow. The presence of the BCR/ABL1 fusion gene within both cellular populations in this case confirmed the extramedullary disease represented a localized T lymphoid/myeloid bilineal blastic transformation of CML. After 3 courses of combined chemotherapy plus tyrosine kinase inhibitor treatment, the mass was completely regressed with a 3-log decrease in BCR/ABL1 transcript from baseline. Five months after the diagnosis, the patient showed diminished vision, hand tremors, and weakness of lower extremities. Flow cytometric immunophenotyping of cerebrospinal fluid revealed the presence of myeloid blasts. An isolated central nervous system relapse of leukemia was identified. Following high-dose systemic and intrathecal chemotherapy, the patient continued to do well.Conclusions:The possibility of extramedullary blast crisis as an initial presentation in patients with CML should be considered. Further, an isolated central nervous system blast crisis should be considered if neurological symptoms evolve in patients who have shown a good response to therapy.

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