scholarly journals Utilization of a chloroplast membrane sulfolipid as a major internal sulfur source for protein synthesis in the early phase of sulfur starvation in Chlamydomonas reinhardtii

FEBS Letters ◽  
2007 ◽  
Vol 581 (23) ◽  
pp. 4519-4522 ◽  
Author(s):  
Koichi Sugimoto ◽  
Norihiro Sato ◽  
Mikio Tsuzuki
2006 ◽  
Vol 72 (5) ◽  
pp. 3524-3530 ◽  
Author(s):  
Kahli M. Weir ◽  
Tara D. Sutherland ◽  
Irene Horne ◽  
Robyn J. Russell ◽  
John G. Oakeshott

ABSTRACT In this paper we describe isolation of a bacterium capable of degrading both isomers of the organochloride insecticide endosulfan and its toxic metabolite, endosulfate. The bacterium was isolated from a soil microbial population that was enriched with continuous pressure to use endosulfate as the sole source of sulfur. Analysis of the 16S rRNA sequence of the bacterium indicated that it was an Arthrobacter species. The organochloride-degrading activity was not observed in the presence of sodium sulfite as an alternative sulfur source, suggesting that the activity was part of the sulfur starvation response of the strain. A gene, ese, encoding an enzyme capable of degrading both isomers of endosulfan and endosulfate was isolated from this bacterium. The enzyme belongs to the two-component flavin-dependent monooxygenase family whose members require reduced flavin for activity. Nuclear magnetic resonance analyses identified the metabolite of endosulfan as endosulfan monoalcohol and the metabolite of endosulfate as endosulfan hemisulfate. The ese gene was located in a cluster of 10 open reading frames encoding proteins with low levels of sulfur-containing amino acids. These open reading frames were organized into two apparent divergently orientated operons and a gene encoding a putative LysR-type transcriptional regulator. The operon not containing ese did contain a homologue whose product exhibited 62% amino acid identity to the ese-encoded protein.


Development ◽  
1974 ◽  
Vol 32 (2) ◽  
pp. 287-295
Author(s):  
Francine Rozenfeld

During their growth, fresh-water sponges release into the medium a dialysable inhibitor (gemmulostasin) which reversibly blocks development of the gemmules at an early phase, prior to the first mitoses. The incorporation of [3H]labelled precursors into DNA, RNA and proteins has been measured throughout development, in the presence or absence of inhibitor. Autoradiographic controls of the nuclear incorporation of [3H]thymidine have been made. Gemmulostasin erases the peak of [3H]thymidine incorporation that otherwise occurs just before the first mitoses. Its overall effect is to bring about, either directly or indirectly, a high peak in the incorporation of [3H]uridine and [3H]leucine at a time when the incorporation of these precursors is low in the controls. It is suggested that a causal relation exists between these phenomena.


1976 ◽  
Vol 20 (3) ◽  
pp. 639-654
Author(s):  
K.W. Farrell

The behaviour of a pool of flagellar precursors, assayed by the ability of cells to regenerate flagella in the absence of de novo protein synthesis, has been examined during organelle morphogenesis in the biflagellate alga Chlamydomonas. The results demonstrate that flagellar elongation can continue even when this pool is apparently empty and suggest that 2 sources of precursors are available to the regenerating flagella: those pre-existing in the cellular pool and those synthesized de novo. Further evidence for this was obtained by subjecting regenerating cells to pulses of cycloheximide. Cells exposed to this drug during the first 60 min post deflagellation formed only half-length (5-mum) flagella, whereas a pulse administered after this point allowed the formation of longer flagella and suggested that some de novo protein synthesis was required for the formation of full-length flagella, although it was not a prerequisite for the initiation of regeneration. In addition, it was found that, subsequent to the removal of the cycloheximide, flagellar regeneration did not recommence immediately, but was delayed for a period of approximately 45 min, irrespective of length of flagella formed prior to drug inhibition. The nature of this cycloheximide-induced delay is unclear and certain alternatives, based on the exhaustion of structural/regulatory components are considered. Although it is not possible to distinguish between these alternatives, tubulin is not the limiting component, since a pool of this protein is present when flagellar elongation is prevented by cycloheximide.


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