Heat stress in the presence of low RNA polymerase activity increases chromosome copy number of Escherichia coli

Summary A temperature shift-up accompanied by a reduction in RNA polymerase activity in Escherichia coli causes an increased rate of initiation leading to a 1.7- to 2.2-fold increase in chromosome copy number. A temperature shift-up without a reduction in polymerase activity induces only a transient non-scheduled initiation of chromosome replication caused by heat shock with no detectable effect on chromosome copy number.     

Environmentally constrained mutation and adaptive evolution in Salmonella

The relationship between environment and mutation is complex [1]. Claims of Lamarkian mutation [2] have proved unfounded [3], [4] and [5]; it is apparent, however, that the external environment can influence the generation of heritable variation, through either direct effects on DNA sequence [6] or DNA maintenance and copying mechanisms [7], [8], [9] and [10], or as a consequence of evolutionary processes [11], [12], [13], [14], [15] and [16]. The spectrum of mutational events subject to environmental influence is unknown [6] and precisely how environmental signals modulate mutation is unclear. Evidence from bacteria suggests that a transient recombination-dependent hypermutational state can be induced by starvation [5]. It is also apparent that chnages in the mutability of specific loci can be influenced by alterations in DNA topology [10] and [17]. Here we describe a remarkable instance of adaptive evolution in Salmonella which is caused by a mutation that occurs in intermediate-strength osmotic environments. We show that the mutation is not ‘directed’ and describe its genetic basis. We also present compelling evidence in support of the hypothesis that the mutational event is constrained by signals transmitted from the external environment via changes in the activity of DNA gyrase.     

Dimeric chromenes and mixed dimers of a chromene with euparin from Encelia canescens

The investigation of Encelia canescens afforded, in addition to several known compounds, four new dimeric p-hydroxyacetophenone derivatives, two epimeric chromene dimers and two epimeric mixed dimers of euparin and encecalin. Furthermore, derivatives of tremetone and of encecalin were present. The structures were elucidated hy high field ¹H NMR spectroscopy.     

Orthologs of key vertebrate neural genes are expressed during neurogenesis in the annelid Platynereis dumerilii

SUMMARY The molecular mechanisms underlying the formation and patterning of the nervous system are relatively poorly understood for lophotrochozoans (like annelids) as compared with ecdysozoans (especially Drosophila ) and deuterostomes (especially vertebrates). Therefore, we have undertaken a candidate gene approach to study aspects of neurogenesis in a polychaete annelid Platynereis dumerilii . We determined the spatiotemporal expression for Platynereis orthologs of four genes ( SoxB, Churchill, prospero / Prox , and SoxC) known to play key roles in vertebrate neurogenesis. During Platynereis development, SoxB is expressed in the neuroectoderm and its expression switches off when committed neural precursors are formed. Subsequently, Prox is expressed in all differentiating neural precursors in the central and peripheral nervous systems. Finally, SoxC and Churchill are transcribed in patterns consistent with their involvement in neural differentiation. The expression patterns of Platynereis SoxB and Prox closely resemble those in Drosophila and vertebrates—this suggests that orthologs of these genes play similar neurogenic roles in all bilaterians. Whereas Platynereis SoxC , like its vertebrate orthologs, plays a role in neural cell differentiation, related genes in Drosophila do not appear to be involved in neurogenesis. Finally, conversely to Churchill in Platynereis , vertebrate orthologs of this gene are expressed during neuroectoderm formation, but not later during nerve cell differentiation; in the insect lineage, homologs of these genes have been secondarily lost. In spite of such instances of functional divergence or loss, the present study shows conspicuous similarities in the genetic control of neurogenesis among bilaterians. These commonalities suggest that key features of the genetic program for neurogenesis are ancestral to bilaterians.     

Galectin 9 is the sugar-regulated urate transporter/channel UAT

UAT, also designated galectin 9, is a multifunctional protein that can function as a urate channel/transporter, a regulator of thymocyte-epithelial cell interactions, a tumor antigen, an eosinophil chemotactic factor, and a mediator of apoptosis. We review the evidence that UAT is a transmembrane protein that transports urate, describe our molecular model for this protein, and discuss the evidence from epitope tag and lipid bilayer studies that support this model of the transporter. The properties of recombinant UAT are compared with those of urate transport into membrane vesicles derived from proximal tubule cells in rat kidney cortex. In addition, we review channel functions predicted by our molecular model that resulted in the novel finding that the urate channel activity is regulated by sugars and adenosine. Finally, the presence and possible functions of at least 4 isoforms of UAT and a closely related gene hUAT2 are discussed. Published in 2004.