The Growth of the Shoot Apex of Chenopodium rubrum L. Treated with a Florigenic Extract from Flowering Tobacco Plants: Preliminary Anatomical Observations

Anatomical changes in the shoot apex of Chenopodium rubrum L.treated with an extract from flowering tobacco plants and cultivatedin non-inductive conditions are described. They are comparedwith the anatomy of non-treated vegetative apices and with apicesof plants induced with a short day. Treatment with the extractresulted in both activation of cell division in the upper partof the apex and in apex elongation. Acceleration of leaf primordiainitiation and stimulation of branching took place. The effectcorresponds to the sequence of changes in photoperiodically-inducedplants but is more pronounced. Elongation following 10^–4M GA₃ treatment was of a differentnature; there was only a slight stimulation in the upper partof the apex in contrast with a strong stimulation of growthin length in the lower internodes. These preliminary resultssuggest a similarity between apical changes evoked by a stimulusproduced by short days and an exogenously applied floral stimulus.The changes differed from those caused by exogenous phytohormones. Key words: Chenopodium rubrum, florigen, shoot apex     

The phospholipid code: a key component of dying cell recognition,tumor progression and host–microbe interactions

A significant effort is made by the cell to maintain certain phospholipids at specific sites. It is well described that proteins involved in intracellular signaling can be targeted to the plasma membrane and organelles through phospholipid-binding domains. Thus, the accumulation of a specific combination of phospholipids, denoted here as the ‘phospholipid code'', is key in initiating cellular processes. Interestingly, a variety of extracellular proteins and pathogen-derived proteins can also recognize or modify phospholipids to facilitate the recognition of dying cells, tumorigenesis and host–microbe interactions. In this article, we discuss the importance of the phospholipid code in a range of physiological and pathological processes.     

Characterization of the effect of LPS on dendritic cell subset discrimination in spleen

The Gram‐negative bacterial endotoxin lipopolysaccharide (LPS) is a potent inflammatory mediator and a leading cause of bacterial sepsis. While LPS is known to activate antigen‐presenting cells, here we find that LPS down‐regulates expression of CD11c and CD11b on splenic dendritic cell subsets, thus confounding the ability to identify these subsets following treatment. This has implications with regard to tracking the response to LPS in terms of the cell subsets involved, and should be considered whenever such studies are undertaken.