The dark side of visual attention

The limited capacity of neural processing restricts the number of objects and locations that can be attended to. Selected events are readily enhanced: the bright side of attention. However, such focal processing comes at a cost, namely, functional blindness for unattended events: the dark side of visual attention. Recent work has advanced our understanding of the neural mechanisms that facilitate visual processing, as well as the neural correlates of unattended, unconscious visual events. Also, new results have revealed how attentional deployment is optimized by non-visual factors such as behavioral set, past experience, and emotional salience.     

The dark side of green fluorescent protein

Here, severe interference of chlorophyll with green fluorescent protein (GFP) fluorescence is described for medicago (Medicago truncatula), rice (Oryza sativa) and arabidopsis (Arabidopsis thaliana). This interference disrupts the proportional relationship between GFP content and fluorescence that is intrinsic to its use as a quantitative reporter. The involvement of chlorophyll in the loss of GFP fluorescence with leaf age was shown in vivo, by the removal of chlorophyll through etiolation or by ethanol extraction, and in vitro, by titration of a GFP solution with chlorophyll solutions of various concentrations. A substantial decrease in fluorescence in early development of medicago and rice leaves correlated with chlorophyll accumulation. In all three species tested, removal of chlorophyll yielded up to a 10-fold increase in fluorescence. Loss of GFP fluorescence in vitro was 4-fold greater for chlorophyll b than for chlorophyll a. Differences exist between plant species for the discrepancy between apparent GFP fluorescence and its actual level in green tissues. Substantial errors in estimating promoter activity from GFP fluorescence can occur if pigment interference is not considered.     

The dark side of cohesin: the carcinogenic point of view

Genome instability is a hallmark of cancer cells and how it arises is still not completely understood. Correct chromosome segregation is a pre-requisite for preserving genome integrity. Cohesin helps to ensure faithful chromosome segregation during cell cycle, however, much evidence regarding its functions have come to light over the last few years and suggest that cohesin plays multiple roles in the maintenance of genome stability. Here we review our rapidly increasing knowledge on the involvement of cohesin pathway in genome stability and cancer.     

The dark side of fly TNF

The fruit fly Drosophila is an important model for biological research; however, due to its relatively short lifespan its relevance in cancer research is often questioned. Nevertheless, among many other intriguing Drosophila models, scribble group mutants provided early evidence for the existence of tumour suppressor genes and their importance in mammalian systems is beginning to emerge. In this review, I discuss recent advances in our understanding of the phenotypes of scrib group gene mutants, in which the activation of JNK signaling plays a crucial role. Several mechanisms can account for the activation of JNK within scrib group mutant cells, including a mechanical stress triggered by the loss of polarity, cell competition, intrinsic tumour suppression by autonomous production of Eiger, and an inflammatory response mediated by Eiger-producing haemocytes. Eiger, the sole Drosophila homolog of tumour necrosis factor, is emerging as a 'danger signal' initiated upon the presence of external pathogens, damaged tissues, and the appearance of pre-malignant cells. Remarkably, in the presence of the Ras oncoprotein Eiger can act as a tumor promoter by stimulating invasive migration and delaying the onset of metamorphosis.     

The dark side of C5a in sepsis

Sepsis is a major clinical problem for which therapeutic interventions have been largely unsuccessful, in spite of promising strategies that were successful in animals, especially rodents. There is new evidence that sepsis causes excessive activation of the complement system and that this induces paralysis of innate immune functions in phagocytic cells due to effects of the powerful complement-activation product, C5a. This review describes our present understanding of how and why sepsis is a life-threatening condition and how it might be more effectively treated.     

Membrane phospholipids and the dark side of vision

The key step in the visual pigment regeneration process is an enzyme-catalyzedtrans tocis retinoid isomerization reaction. This reaction is of substantial general interest, because it requires the input of metabolic energy. The energy is needed because the 11-cis-retinoid reaction products are approximately 4kcal/mol higher in energy than their all-trans congeners. In the retinal pigment epithelium a novel enzymatic system has been discovered which is capable of converting all-trans-retinol into all-trans retinyl esters, by means of a lecithin retinol acyl transferase (LRAT), followed by the direct processing of the ester into 11-cis-retinol. In this process the free energy of hydrolysis of a retinyl ester, estimated to be approximately –5kcal/mol, is coupled to the endothermic (+4kcal/mol) isomerization reaction, resulting in an overall exothermic process. The overall process is analogous to ATP-dependent group transfer reactions, but here the energy is provided by the membrane phospholipids. This process illustrates a new role for membranes: they can serve as an energy source.     

Lymphoid malignancies: the dark side of B-cell differentiation

When the regulation of B-cell differentiation and activation is disrupted, lymphomas and leukaemias can occur. The processes that normally create immunoglobulin diversity might be misdirected, resulting in oncogenic chromosomal translocations that block differentiation, prevent apoptosis and/or promote proliferation. Prolonged or unregulated antigenic stimulation might contribute further to the development and progression of some malignancies. Lymphoid malignancies often resemble normal stages of B-cell differentiation, as shown by molecular techniques such as gene-expression profiling. The similarities and differences between malignant and normal B cells indicate strategies for the treatment of these cancers.