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The production of singlet oxygen is typically associated with inefficient dissipation of photosynthetic energy or can arise from light reactions as a result of accumulation of chlorophyll precursors as observed in fluorescent (flu)-like mutants. Such photodynamic production of singlet oxygen is thought to be involved in stress signaling and programmed cell death. Here we show that transcriptomes of multiple stresses, whether from light or dark treatments, were correlated with the transcriptome of the flu mutant. A core gene set of 118 genes, common to singlet oxygen, biotic and abiotic stresses was defined and confirmed to be activated photodynamically by the photosensitizer Rose Bengal. In addition, induction of the core gene set by abiotic and biotic selected stresses was shown to occur in the dark and in nonphotosynthetic tissue. Furthermore, when subjected to various biotic and abiotic stresses in the dark, the singlet oxygen-specific probe Singlet Oxygen Sensor Green detected rapid production of singlet oxygen in the Arabidopsis (Arabidopsis thaliana) root. Subcellular localization of Singlet Oxygen Sensor Green fluorescence showed its accumulation in mitochondria, peroxisomes, and the nucleus, suggesting several compartments as the possible origins or targets for singlet oxygen. Collectively, the results show that singlet oxygen can be produced by multiple stress pathways and can emanate from compartments other than the chloroplast in a light-independent manner. The results imply that the role of singlet oxygen in plant stress regulation and response is more ubiquitous than previously thought.

Metastatic spread of cancer cells is the leading cause of mortality from cancer. Metastatic cancer cells must penetrate through several barriers to escape the primary tumor and gain entry into the bloodstream in order to spread to other tissues. It is believed that invasive cancer cells penetrate these barriers by forming specialized F-actin rich protrusions called invadopodia that localize matrix degrading activity to cell-substrate contact points. Invadopodia gain their protrusive ability by combining the physical force generated by actin polymerization with the chemical activity of matrix degradation. Accumulating data over the past few years have shed light on the molecular mechanisms as well as kinase signaling pathways that regulate the complex process of actin polymerization in invadopodia. Here we review some of these mechanisms, the signaling pathways that regulate this process, as well as the in vivo relevance of invadopodial structures. Understanding the mechanisms that govern invadopodia formation and function is an essential step in the prevention of cancer invasion and metastasis.