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Here we report that petal tissue was responsible for the bulk of the phenylpropanoid emission. The activity of S-adenosyl-i-methionine:(iso)eugenol O-methyltransferase (IEMT), a nove1 enzyme that catalyzes the methylation of the para-4'-hydroxyl of both eugenol and (iso)eugenol to methyleugenol and isomethyleugenol, respectively, was also highest i n petal tissue. IEMT activity was absent from floral tissues of plants not emitting (iso)methyleugenol. A C. breweri cDNA clone encoding IEMT was isolated, and its sequence was shown t o have 70% identity t o S-adenosyl-L-methionine:caffeic acid Omethyltransferase. l h e protein encoded by this cDNA can use eugenol and isoeugenol as substrates, but not caffeic acid. Steadystate IEMT mRNA levels were positively correlated with levels of IEMT activity in the tissues, and no IEMT mRNA was observed in flowers that do not emit (iso)methyleugenol. Overall, the data show that the floral emission of (iso)methyleugenol is controlled at the site of emission, that a positive correlation exists between volatile emission and IEMT activity, and that control of the level of IEMT activity is exerted at a pretranslational step.Flowers of many plants attract pollinators by producing and emitting a complex mixture of low-molecular-weight volatile compounds. Floral scents may function as both long-and short-distance attractants and nectar guides to a variety of animal pollinators (for review, see Dobson, 1993). Since insects are able to distinguish between complex floral scent mixtures, discriminatory visitation based on floral scent has important implications for population structure and reproductive isolation (Dodson et al

Vascular disrupting agents (VDAs), or endothelial disrupting agents, attempt to exploit the vascular endothelium that supplies rapidly dividing neoplasms. Unlike antiangiogenesis agents (e.g. the monoclonal antibody bevacizumab; and tyrosine kinase inhibitors sorafenib and sunitinib) that disrupt endothelial cell survival mechanisms and the development of a new tumor blood supply, VDAs are designed to disrupt the already established abnormal vasculature that supports tumors, by targeting their dysmorphic endothelial cells. Tumor vascular endothelium is characterized by its increased permeability, abnormal morphology, disorganized vascular networks, and variable density. VDAs induce rapid shutdown of tumor blood supply, causing subsequent tumor death from hypoxia and nutrient deprivation. The safety profile of this class of compounds is more indicative of agents that are indeed 'vascularly' active. For example, VDAs can cause: acute coronary and other thrombophlebitic syndromes; alterations in blood pressure, heart rate, and ventricular conduction; transient flush and hot flashes; neuropathy; and tumor pain. Despite these cardiovascular concerns some patients have benefited from VDAs in early clinical trials. Further drug development of VDAs must include the combination of these agents with other novel biological agents, cytotoxic chemotherapy, and radiotherapy. Close monitoring of patients receiving VDAs for any cardiovascular toxicity is imperative.

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Biological engineers often find it useful to communicate using diagrams. These diagrams can include information both about the structure of the nucleic acid sequences they are engineering and about the functional relationships between features of these sequences and/or other molecular species. A number of conventions and practices have begun to emerge within synthetic biology for creating such diagrams, and the Synthetic Biology Open Language Visual (SBOL Visual) has been developed as a standard to organize, systematize, and extend such conventions in order to produce a coherent visual language. Here, we describe SBOL Visual version 2, which expands previous diagram standards to include new functional interactions, categories of molecular species, support for families of glyph variants, and the ability to indicate modular structure and mappings between elements of a system. SBOL Visual 2 also clarifies a number of requirements and best practices, significantly expands the collection of glyphs available to describe genetic features, and can be readily applied using a wide variety of software tools, both general and bespoke.

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Myocardial stunning, known as stress cardiomyopathy, broken-heart syndrome, transient left ventricular apical ballooning, and Takotsubo cardiomyopathy, has been reported after many extracardiac stressors, but not following chemotherapy. We report 2 cases with characteristic electrocardiographic and echocardiographic features following combined modality therapy with combretastatin, a vascular-disrupting agent being studied for treatment of anaplastic thyroid cancer. In 1 patient, an ECG performed per protocol 18 hours after drug initiation showed deep, symmetric T-wave inversions in limb leads I and aVL and precordial leads V 2 through V 6 . Echocardiography showed mildly reduced overall left ventricular systolic function with akinesis of the entire apex. The patient had mild elevations of troponin I. Coronary angiography revealed no epicardial coronary artery disease. The electrocardiographic and echocardiographic abnormalities resolved after several weeks. The patient remains stable from a cardiovascular standpoint and has not had a recurrence during follow-up. An electrocardiogram performed per protocol in a second patient showed deep, symmetric T-wave inversions throughout the precordial leads and a prolonged QT interval. Echocardiography showed mildly reduced left ventricular function with hypokinesis of the apical-septal wall. Acute coronary syndrome was ruled out, and both the electrocardiographic and echocardiographic changes resolved at follow-up. Although the patient remained pain-free without recurrence of anginal symptoms during long-term follow-up, the patient developed progressive malignancy and died. IntroductionMyocardial stunning, known as stress cardiomyopathy, broken heart syndrome, left ventricular apical ballooning, and Takotsubocardiomyopathyis defined as: left ventricular apical ballooning on echocardiography or ventriculography; no angiographic stenoses > 50%; and no history of known cardiomyopathy. While the patient in the first of our 2 case reports fulfills these criteria, the second patient had a positive stress test following the incident but did not undergo coronary angiography, so ischemic heart disease was not excluded.Combretastatin may precipitate acute coronary syndrome. 1 A 57-year-old male with pancreatic cancer developed chest pain 80 minutes after combretastatin, and ECG showed acute myocardial infarction. Coronary angiography demonstrated an occluded distal left anterior descending artery. A 77-year-old male developed ECG changes and elevated troponin I following combretastatin. Coronary angiography revealed 2-vessel coronary artery disease.

We describe a synthetic genetic circuit for controlling asymmetric cell division in E. coli in which a progenitor cell creates a differentiated daughter cell while retaining its original phenotype. Specifically, we engineered an inducible system that can bind and segregate plasmid DNA to a single position in the cell. Upon cell division, co-localized plasmids are kept by one and only one of the daughter cells. The other daughter cell receives no plasmid DNA and is hence irreversibly differentiated from its sibling. In this way, we achieved asymmetric cell division through asymmetric plasmid partitioning. We then used this system to achieve physical separation of genetically distinct cells by tying motility to differentiation. Finally, we characterized an orthogonal inducible circuit that enables the simultaneous asymmetric partitioning of two plasmid species, resulting in cells that have four distinct differentiated states. These results point the way towards engineering multicellular systems from prokaryotic hosts.