Spontaneous and induced reversion rates in a double heterozygous mutant of Nicotiana tabacum var. xanthi n.c. —Dose-response relationship

The ability of the double heterozygous mutant a₁⁺/a₁a₂⁺/a₂(greenish-yellow) to revert phenotypically towards green was used to quantify the dose-response relationship at 0, 8, 16, 32, 64, 128 and 256 R of gamma-rays from a ⁶⁰Co-source. All the studies undertaken up to now on the genetic nature of the events responsible for the phenotypic reversion suggest that the changes take place mostly at locus a₁⁺−a₁.The present experiment was split into two parts: a low-dose (0–64 R) and a higher-dose (64–256 R) analysis, in which the responses were quadratic and linear, respectively.The spontaneous reversion rate was estimated to be 10⁻⁵.     

Testing for the presence of a partially penetrant dominant gene

Favor, in the Appendix to a paper by Ehling and his collaborators (Ehling et al., 1982), develops a method that tests for the presence of a partially penetrant dominant cataract mutation in a suspected parent (showing lens opacity) outcrossed to a homozygous strain-101 mouse when no individual with lens opacity is observed in the progeny. This method, based on the Chi-square distribution, is examined as to the validity of the Normal approximation. An alternative procedure is discussed.     

Fungal hydroquinones contribute to brown rot of wood

The fungi that cause brown rot of wood initiate lignocellulose breakdown with an extracellular Fenton system in which Fe(2+) and H(2)O(2) react to produce hydroxyl radicals (.OH), which then oxidize and cleave the wood holocellulose. One such fungus, Gloeophyllum trabeum, drives Fenton chemistry on defined media by reducing Fe(3+) and O(2) with two extracellular hydroquinones, 2,5-dimethoxyhydroquinone (2,5-DMHQ) and 4,5-dimethoxycatechol (4,5-DMC). However, it has never been shown that the hydroquinones contribute to brown rot of wood. We grew G. trabeum on spruce blocks and found that 2,5-DMHQ and 4,5-DMC were each present in the aqueous phase at concentrations near 20 microM after 1 week. We determined rate constants for the reactions of 2,5-DMHQ and 4,5-DMC with the Fe(3+)-oxalate complexes that predominate in wood undergoing brown rot, finding them to be 43 l mol(-1) s(-1) and 65 l mol(-1) s(-1) respectively. Using these values, we estimated that the average amount of hydroquinone-driven .OH production during the first week of decay was 11.5 micromol g(-1) dry weight of wood. Viscometry of the degraded wood holocellulose coupled with computer modelling showed that a number of the same general magnitude, 41.2 micromol oxidations per gram, was required to account for the depolymerization that occurred in the first week. Moreover, the decrease in holocellulose viscosity was correlated with the measured concentrations of hydroquinones. Therefore, hydroquinone-driven Fenton chemistry is one component of the biodegradative arsenal that G. trabeum expresses on wood.     

Hydroxycinnamic acid amides and ripening to flower of Nicotiana tabacum var. xanthi n.c.

Two kinds of hydroxycinnamic derivatives can be found in tobacco: esters and amides. They do not accumulate in the same way during development. Esters, especially chlorogenic acids, are always present in all organs, whereas amides are observed only during certain periods in specific organs (from 47 days after sowing, in apical leaves, anthers and ovaries). A relationship has been found between accumulation of amides and flowering of plants grown at 20°C. By comparing amide accumulation as well as leaf emergence rate, both at a temperature that allows flowering (20°C) and at a temperature that inhibits flowering (30°C), it appears that amides begin to accumulate whenever a plant is ripening to flower.     

SpoT governs Legionella pneumophila differentiation in host macrophages

During its life cycle, Legionella pneumophila alternates between a replicative and a transmissive state. To determine their contributions to L. pneumophila differentiation, the two ppGpp synthetases, RelA and SpoT, were disrupted. Synthesis of ppGpp was required for transmission, as relA spoT mutants were killed during entry to and exit from macrophages. RelA, which senses amino acid starvation induced by serine hydroxamate, is dispensable in macrophages, as relA mutants spread efficiently. SpoT monitors fatty acid biosynthesis (FAB), since following cerulenin treatment, wild-type and relA strains expressed the flaA transmissive gene, but relA spoT mutants did not. As in Escherichia coli , the SpoT response to FAB perturbation likely required an interaction with acyl-carrier protein (ACP), as judged by the failure of the spoT-A413E allele to rescue transmissive trait expression of relA spoT bacteria. Furthermore, SpoT was essential for transmission between macrophages, since secondary infections by relA spoT mutants were restored by induction of spoT , but not relA . To resume replication, ppGpp must be degraded, as mutants lacking spoT hydrolase activity failed to convert from the transmissive to the replicative phase in either bacteriological medium or macrophages. Thus, L. pneumophila requires SpoT to monitor FAB and to alternate between replication and transmission in macrophages.     

Legionella pneumophila couples fatty acid flux to microbial differentiation and virulence

During its life cycle, Legionella pneumophila alternates between at least two phenotypes: a resilient, infectious form equipped for transmission and a replicative cell type that grows in amoebae and macrophages. Considering its versatility, we postulated that multiple cues regulate L. pneumophila differentiation. Beginning with a Biolog Phenotype MicroArray screen, we demonstrate that excess short-chain fatty acids (SCFAs) trigger replicative cells to cease growth and activate their panel of transmissive traits. To co-ordinate their response to SCFAs, L. pneumophila utilizes the LetA/LetS two-component system, but not phosphotransacetylase or acetyl kinase, two enzymes that generate high-energy phosphate intermediates. Instead, the stringent response enzyme SpoT appears to monitor fatty acid biosynthesis to govern transmission trait expression, as an altered distribution of acylated acyl carrier proteins correlated with the SpoT-dependent differentiation of cells treated with either excess SCFAs or the fatty acid biosynthesis inhibitors cerulenin and 5-(tetradecyloxy)-2-furoic acid. We postulate that, by exploiting the stringent response pathway to couple cellular differentiation to its metabolic state, L. pneumophila swiftly acclimates to stresses encountered in its host or the environment, thereby enhancing its overall fitness.     

ppGpp: magic beyond RNA polymerase

During stress, bacteria undergo extensive physiological transformations, many of which are coordinated by ppGpp. Although ppGpp is best known for enhancing cellular resilience by redirecting the RNA polymerase (RNAP) to certain genes, it also acts as a signal in many other cellular processes in bacteria. After a brief overview of ppGpp biosynthesis and its impact on promoter selection by RNAP, we discuss how bacteria exploit ppGpp to modulate the synthesis, stability or activity of proteins or regulatory RNAs that are crucial in challenging environments, using mechanisms beyond the direct regulation of RNAP activity.     

Genetic effects on the a1+a1a2+a2 system of tobacco over a uranous outcrop in lauragais (Aude,France)

2 experiments were designed to study the reversion rate values of the $\text{a}{}_1{}^{\mathrm{+}}\text{a}{}_1\text{a}{}_2{}^{\mathrm{+}}\text{a}{}_2$ system of tobacco over the Lagravette uranous outcrop for dose rates ranging close to the background level, and so to detect an eventual threshold effect. Both experiments apparently led to the same conclusion: for the genetic system involved, there seemed to be a threshold somewhere between 0.291 and 0.449 mrd/h, i.e., 2.55 and 3.93 rd/y. It also appeared that, above the threshold, the dose—response relationship could be linear.     

ppGpp Conjures Bacterial Virulence

Summary: Like for all microbes, the goal of every pathogen is to survive and replicate. However, to overcome the formidable defenses of their hosts, pathogens are also endowed with traits commonly associated with virulence, such as surface attachment, cell or tissue invasion, and transmission. Numerous pathogens couple their specific virulence pathways with more general adaptations, like stress resistance, by integrating dedicated regulators with global signaling networks. In particular, many of nature''s most dreaded bacteria rely on nucleotide alarmones to cue metabolic disturbances and coordinate survival and virulence programs. Here we discuss how components of the stringent response contribute to the virulence of a wide variety of pathogenic bacteria.