Transcriptomic Signature of Human Embryonic Thyroid Reveals Transition From Differentiation to Functional Maturation

The human thyroid gland acquires a differentiation program as early as weeks 3–4 of embryonic development. The onset of functional differentiation, which manifests by the appearance of colloid in thyroid follicles, takes place during gestation weeks 10–11. By 12–13 weeks functional differentiation is accomplished and the thyroid is capable of producing thyroid hormones although at a low level. During maturation, thyroid hormones yield increases and physiological mechanisms of thyroid hormone synthesis regulation are established. In the present work we traced the process of thyroid functional differentiation and maturation in the course of human development by performing transcriptomic analysis of human thyroids covering the period of gestation weeks 7–11 and comparing it to adult human thyroid. We obtained specific transcriptomic signatures of embryonic and adult human thyroids by comparing them to non-thyroid tissues from human embryos and adults. We defined a non-TSH (thyroid stimulating hormone) dependent transition from differentiation to maturation of thyroid. The study also sought to shed light on possible factors that could replace TSH, which is absent in this window of gestational age, to trigger transition to the emergence of thyroid function. We propose a list of possible genes that may also be involved in abnormalities in thyroid differentiation and/or maturation, hence leading to congenital hypothyroidism. To our knowledge, this study represent the first transcriptomic analysis of human embryonic thyroid and its comparison to adult thyroid

Mechanism of SOS-induced targeted and untargeted mutagenesis in E. coli.

This paper retraces the evolution of hypotheses concerning mechanisms of SOS induced mutagenesis. Moreover, it reports some recent data which support a new model for the mechanism of targeted and untargeted mutagenesis in E. coli. In summary, the SOS mutator effect, which is responsible for untargeted mutagenesis and perhaps for the misincorporation step in targeted mutagenesis, is believed to involve a fidelity function associated with DNA polymerase III and does not require the umuC gene product. umuC and umuD gene products are probably required specifically for elongation of DNA synthesis past blocking lesions, i.e. to allow mutagenic replication of damaged DNA. © 1985 Masson, Paris.SCOPUS: re.jinfo:eu-repo/semantics/publishe

Mechanisms of protection of γirradiated bacteriophage λ by proflavine

The protective effect of proflavine on γirradiated bacteriophage λ and its isolated DNA was investigated under conditions of predominantly indirect or direct effects. In both conditions addition of small amounts of the dye during irradiation of phage or DNA was shown to enhance their biological activity. Protection against indirect effects results probably from extensive scavenging of radioinduced water radicals within the medium. On the other hand the results obtained at -196°C, with irradiated DNA-proflavine complexes, imply the existence of a long-range transfer of the primary radiation damage of DNA towards the intercalated molecules of proflavine. A mechanism for the protective effect of proflavine against the direct effect of ionizing radiation on biologically active DNA is suggested. © 1975 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

La proflavine est un protecteur du DNA contre les radiations ionisantes: étude réalisée sur le bactériophage l

Doctorat en Sciencesinfo:eu-repo/semantics/nonPublishe

La proflavine est un protecteur du DNA contre les radiations ionisantes: étude réalisée sur le bactériophage l

Doctorat en Sciencesinfo:eu-repo/semantics/nonPublishe

Role of RecA protein in untargeted UV mutagenesis of bacteriophage λ: Evidence for the requirement for the dinB gene

Untargeted UV mutagenesis of bacteriophage λ - i.e. the increased recovery of λ mutants when unirradiated λ infects UV-irradiated Escherichia coli - is thought to be mediated by a transient decrease in DNA replication fidelity, generating mutations in the newly synthesized strands. Using the bacteriophage λ cI857 → λ c mutation system, we provide evidence that the RecA protein, shown previously to be required for this mutagenic pathway, is no longer needed when the LexA protein is inactivated by mutation. We suggest that the error-prone DNA replication responsible for UV-induced untargeted mutagenesis is turned on by the presence of replication-blocking lesions in the host cell DNA and that the RecA protein is required only to derepress the relevant din gene(s). This is in contrast to mutagenesis of irradiated bacteria or irradiated phage λ, in which activated RecA protein has a second role in mutagenesis in addition to the cleavage of the LexA protein. Among the tested din genes, the dinB gene product (in addition to the uvrA and uvrB gene products) was found to be required for untargeted mutagenesis of bacteriophage λ. To our knowledge, a phenotype associated with the dinB gene has not been reported previously.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

LA 2 AMINO-PURINE, UN ANALOGUE DE L'ADENINE, INDUIT CHEZ E.COLI UN MECANISME DE REPARATION NON MUTAGENE AGISSANT SUR LES LESIONS ULTRAVIOLETTES DANS L'ADN DOUBLE-BRIN

SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Nature of the SOS mutator activity: Genetic characterization of untargeted mutagenesis in Escherichia coli

SCOPUS: ar.jinfo:eu-repo/semantics/publishe

2-Aminopurine induced DNA repair in E. coli

SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Genetic control of the UV-induced SOS mutator effect in single- and double-stranded DNA phages

SCOPUS: ar.jinfo:eu-repo/semantics/publishe