scholarly journals Use of a promoterless lacZ gene insertion to investigate chitinase gene expression in the marine bacterium Pseudoalteromonas sp. strain S9.

1997 ◽  
Vol 63 (8) ◽  
pp. 2989-2996 ◽  
Author(s):  
S Techkarnjanaruk ◽  
S Pongpattanakitshote ◽  
A E Goodman
2009 ◽  
Vol 3 (9) ◽  
pp. 1064-1069 ◽  
Author(s):  
Marina W Delpin ◽  
Amanda E Goodman

1982 ◽  
Vol 152 (2) ◽  
pp. 829-839
Author(s):  
A M Easton ◽  
R H Rownd

The incompatibility properties of IncFII R plasmid NR1 were compared with those of two of its copy number mutants, pRR12 and pRR21. pRR12 produced an altered incompatibility product and also had an altered incompatibility target site. The target site appeared to be located within the incompatibility gene, which is located more than 1,200 base pairs from the plasmid origin of replication. The incompatibility properties of pRR21 were indistinguishable from those of NR1. Lambda phages have been constructed which contain the incompatibility region of NR1 or of one of its copy mutants fused to the lacZ gene. In lysogens constructed with these phages, beta-galactosidase was produced under the control of a promoter located within the plasmid incompatibility region. Lysogens containing prophages with the incompatibility regions from pRR12 and pRR21 produced higher levels of beta-galactosidase than did lysogens containing prophages with the incompatibility region from the wild-type NR1. The introduction into these inc-lac lysogens of pBR322 plasmids carrying the incompatibility regions of the wild-type or mutant plasmids resulted in decreased levels of beta-galactosidase production. For a given lysogen, the decrease was greater when the pBR322 derivative expressed a stronger incompatibility toward the plasmid from which the fragment in the prophage was derived. This suggested that the incompatibility product acts on its target to repress gene expression in the plasmid replication region.


2009 ◽  
Vol 134 (3) ◽  
pp. 379-386 ◽  
Author(s):  
Bao-Cheng Ma ◽  
Wan-Li Tang ◽  
Li-Yan Ma ◽  
Ling-Ling Li ◽  
Lu-Bin Zhang ◽  
...  

The pathogenic fungus Colletotrichum musae infects developing green bananas (Musa spp. AAA group), but remains latent until the fruit ripens. The aim of this research was to determine whether the appearance of disease symptoms is regulated by chitinase gene expression following treatment of fruit with benzothiadiazole (BTH) and methyl jasmonate (MeJA), and with physical (heat) and chemical (H2O2 and Ca2+-related) treatments. In bananas inoculated with C. musae, BTH and MeJA lowered disease severity and stimulated higher gene expression compared with the untreated controls during ripening. However, in naturally infected bananas, BTH and MeJA treatments slightly reduced transcription of the chitinase gene in green bananas, but they prolonged gene expression in ripe bananas and significantly reduced disease severity. The combination of H2O2 and the NADPH oxidase inhibitor, diphenylene iodonium, down-regulated chitinase gene expression and compromised disease resistance compared with H2O2 alone. Heat treatment (HT) or the combination of HT followed by CaCl2 reduced disease, but only the latter significantly upregulated chitinase gene expression. The combination of HT and a calcium ionophore (A23187) resulted in different disease indicies and different levels of gene expression depending upon the order of application: HT followed by A23187 induced higher gene expression and lower disease. The results suggest that disease resistance of green bananas could be related to high and prolonged levels of chitinase gene expression, and chitinase could be involved in harvested banana's anthracnose resistance activated by different defense pathway signals, such as BTH, MeJA, H2O2, and Ca2+.


Development ◽  
1991 ◽  
Vol 112 (3) ◽  
pp. 807-811 ◽  
Author(s):  
K. Schughart ◽  
C.J. Bieberich ◽  
R. Eid ◽  
F.H. Ruddle

To characterize cis-acting regulatory elements of the murine homeobox gene, Hox-2.2, transgenic mouse lines were generated that contained the LacZ reporter gene under the control of different fragments from the presumptive Hox-2.2 promoter. A promoter region of 3600 base pairs (bp) was identified, which reproducibly directed reporter gene expression into specific regions of developing mouse embryos. At 8.5 days postcoitum (p.c.) reporter gene activity was detected in posterior regions of the lateral mesoderm and, in subsequent developmental stages, expression of the LacZ gene was restricted to specific regions of the developing limb buds and the mesenchyme of the ventrolateral body region. This pattern of Hox-2.2-LacZ expression was found in all transgenic embryos that have been generated with the 3.6 kb promoter fragment (two founder embryos and embryos from five transgenic lines). In addition, embryos from two transgenic mouse lines expressed the reporter gene at low levels in the developing central nervous system (CNS). Our results are consistent with the idea that in addition to their presumptive role in CNS and vertebrae development, Hox-2.2 gene products are involved in controlling pattern formation in developing limbs.


Development ◽  
1993 ◽  
Vol 118 (1) ◽  
pp. 71-82 ◽  
Author(s):  
R. Vogels ◽  
J. Charite ◽  
W. de Graaff ◽  
J. Deschamps

The Hox genes have been proved to be instrumental in establishing the positional identity of cells along the embryonic anteroposterior (A-P) axis. Studying the regulation of these genes is a first step toward elucidating the molecular basis of regionalization during embryogenesis. We report here on the identification of cis-acting elements controlling the expression of Hoxb-7 (Hox-2.3). We show that elements driving A-P restricted gene expression are located within the 3.5 kb proximal upstream sequences of the Hoxb-7 gene. A deletion analysis provides evidence for at least three cis-acting control elements upstream from Hoxb-7, and for cooperative interactions between some of these elements in generating the A-P restricted transgenic pattern. One element, conferring by itself Hox-like expression boundaries to the transgene, has been studied in more detail and found to act in an orientation-and promoter-dependent manner. Together the 3.5 kb sequences proximal to Hoxb-7 mediate A-P restricted Hoxb-7/lacZ gene expression in a domain showing rostral boundaries more posterior than those of Hoxb-7. The evolution throughout embryogenesis of the expression pattern of a transgene carrying these sequences has been analysed and shown to mimick that of the endogenous gene, except for a slight delay in the initial expression. We conclude that the transgenes that we tested, spanning a total of 27 kb genomic sequences, do not reproduce all the features of the Hoxb-7 expression pattern. The differences in expression between Hoxb-7 and the transgenes may reveal an aspect of the Hox regulation for which either remote cis-acting control elements and/or gene clustering is required. Additional features that may have favoured maintenance of clustered organisation during evolution are partial overlap of transcription units with the regulatory regions of the neighbouring genes, and cis-regulatory interactions between multiple Hox genes: not only do cis-acting control elements of the Hoxb-7 gene map in the 3′ untranslated sequences of the Hoxb-8 (Hox-2.4) gene, but our experiments suggest that Hoxb-7 control sequences modulate expression of the Hoxb-8 gene as well.


Author(s):  
Karen E. Broglie ◽  
John J. Gaynor ◽  
Mylene Durand-Tardif ◽  
Richard Broglie

Genetics ◽  
1987 ◽  
Vol 117 (2) ◽  
pp. 173-179
Author(s):  
Gary N Gussin ◽  
Susan Brown ◽  
Karen Matz

ABSTRACT A PRM-cI-lacZ fusion inserted into the b2 region of bacteriophage λ was used to isolate mutations affecting expression of both the λ cI gene and the lacZ gene. One such mutation, a change in the cI initiator codon from AUG to AUA, reduces immunity of a λ prophage to superinfection, and causes a 60-70% reduction in β-galactosidase synthesis, even when repressor is supplied in trans. The effect of the mutation on lacZ gene expression is eliminated in a rho  - bacterial strain, and the mutation has no effect on transcription initiated at PRM in vitro. Therefore, the effects of the mutation are due to premature ρ-dependent termination of transcription in the absence of translation of the cI gene, as if the mutation were a nonsense polar mutation.


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