• Korean Journal of Microbiology
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• v.52 no.1
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• pp.120-124
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• 2016

A certain size of DNA (28-29 kb long) to be packaged into P2-size head and the mutation in sid gene of bacteriophage P4 are the major factors to overcome "P2 sir-associated helper inefficiency". To clarify whether the presence of sid mutation is essential to overcome "P2 sir-associated helper inefficiency" or not, we tested the P4 derivative, P4 delRI::kmr, which is $sid^+$ and whose genome size supposed to be 28.5 kb long in the case of being packaged into $P2_{sir3}$-sized large head. As P4 delRI::kmr showed the low EOP with P2 sir3 lysogen, P4 delRI::kmr phage stock was prepared in P2 sir3 lysogen host to increase the EOP with P2 sir3 lysogen. Through this process, P4 delRI::kmr had been adapted for P2 sir3 lysogen. With a CsCl buoyant equilibrium density gradient experiment and gel electrophoresis of the isolated DNA, it was evident that the adaptation of P4 delRI::kmr for P2 sir3 lysogen was caused by the conformational change of DNA to be packaged into large head. The burst size determination experiments with P4 delRI::kmr phage stock adapted for P2 sir3 lysogen and normal P4 delRI::kmr phage stock showed that not the sid mutation but the size of DNA to be packaged (28-29 kb long) was essential to overcome "P2 sir-associated helper inefficiency".

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.2
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• pp.1043-1047
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• 2013

Although there have been many studies investigating possible associations between the C1653T mutation and risk of HCC, the results have been inconsistent. We conducted searches of the published literature in Pubmed and Embase databases up to January 2013. Seventeen studies with a total of 1,085 HCC cases and 1,365 healthy controls were retrieved. We found a significant association between the C1653T mutation and HCC risk (OR = 2.01, 95%CI= 1.49-2.70). In the subgroup analysis by ethnicity, a significant association was also found in Asians (OR = 2.07, 95%CI= 1.71-2.51). In subgroup analysis by HBV genotype, B and C were linked with development of HCC (B:OR = 2.21, 95%CI= 1.13-4.34; C:OR = 2.26, 95%CI= 1.61-3.16). However, no significant association was found between the C1653T mutation and HCC risk in HBeAg positive cases. In conclusion, this meta-analysis suggests that the C1653T mutation may be associated with susceptibility to HCC.

• Clinical and Experimental Pediatrics
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• v.57 no.2
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• pp.91-95
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• 2014

Griscelli syndrome type 2 (GS2) is a rare autosomal recessive disease caused by mutations in the RAB27A gene. It is characterized by cutaneous hypopigmentation, immunodeficiency, and hemophagocytic lymphohistiocytosis. We describe 2 brothers who had GS2 with clinically diverse manifestations. The elder brother presented with a purely neurological picture, whereas the younger one presented with fever, pancytopenia, hepatosplenomegaly, and erythema nodosum. Considering that cutaneous hypopigmentation was a common feature between the brothers, genetic analysis for Griscelli syndrome was performed. As the elder sibling had died, mutation analysis was only performed on the younger sibling, which revealed a novel homozygous mutation in the RAB27A gene on chromosome 15 showing a single-base substitution (c.136T>A p.F46I). Both parents were heterozygous for the same mutation. This confirmed the diagnosis of GS2 in the accelerated phase in both siblings. The atypical features of GS2 in these cases are a novel mutation, isolated neurological involvement in one sibling, association with erythema nodosum, and 2 distinct clinical presentations in siblings with the same genetic mutation.

• Journal of Microbiology
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• v.43 no.spc1
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• pp.110-117
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• 2005

Salmonella enterica serovar Typhimurium causes human gastroenteritis and a systemic typhoid-like infection in mice. A critical virulence determinant of Salmonella is the ability to invade mammalian cells. The expression of genes required for invasion is tightly regulated by environmental conditions and a variety of regulatory genes. The hilA regulator encodes an OmpR/ToxR family transcriptional regulator that activates the expression of invasion genes in response to both environmental and genetic regulatory factors. Work from several laboratories has highlighted that regulation of hilA expression is a key point for controlling expression of the invasive phenotype. A number of positive regulators of hilA expression have been identified including csrAB, sirA/barA, pstS, hilC/sirC/sprA, fis, and hilD. HilD, an AraC/XylS type transcriptional regulator, is of particular importance as a mutation in hilD results in a 14-fold decrease in chromosomal hilA::Tn5lacZY-080 expression and a 53-fold decrease in invasion of HEp-2 cells. It is believed that HilD directly regulates hilA expression as it has been shown to bind to hilA promoter sequences. In addition, our research group, and others, have identified genes (hilE, hha, pag, and lon) that negatively affect hilA transcription. HilE appears to be an important Salmonella-specific regulator that plays a critical role in inactivating hilA expression. Recent work in our lab has been directed at understanding how environmental signals that affect hilA expression may be processed through a hilE pathway to modulate expression of hilA and the invasive phenotype. The current understanding of this complex regulatory system is reviewed.

• The Korean Journal of Mycology
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• v.19 no.4
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• pp.266-275
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• 1991

The gene CDC70 encoding the${\alpha}-subunit$ of G protein has been known to be a component involved in mating pheromone signalling in the yeast, Saccharomyces cerevisiae. To isolate mutations of the genes involved in the signal transduction, Saccharomyces cerevisiae the strain bearing the cdc70-5 mutation was mutagenized to be forced to recover the ability of colony-formation at restrictive temperature, which means the new mutation can suppress the temperature sensitivity of the cdc70-5 phenotypes. Among these suppressors, $sir^-$ and $mat{\alpha}2^{-}$ mutations are excluded because of no relationship to signal transducer. And the selected suppressors were analyzed for the linkage relationships by the tetrad analysis. Out of fifteen suppressors isolated, twelve were classified into four linkage groups, designated as sga1, sga2, sga3, sga4 by the tetrad analysis. The other three genes were determined for the linkage.