Mutation spectrum in Salmonella induced by environmental tobacco smoke

Zhou, Ran; Yu, Guang; Zhou, Yingqiao; Zeng, Xiaofei

doi:10.1002/(sici)1098-2280(1999)33:3<185::aid-em2>3.0.co;2-t

Cited by 3 publications

(1 citation statement)

References 33 publications

(33 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been reported that G is likely to be misread as a T nucleotide, due to the formation of 8-oxo-dG during NGS sample preparation 22 , 23 ; therefore, it is possible that the sensitivity of G:C > T:A mutation detection was relatively strongly affected by this artificial error. The detection of mutations induced by mutagens that mainly cause G:C > T:A substitution, such as polycyclic aromatic hydrocarbons (PAHs), might be more difficult than detection of mutations caused by other types of mutagens 24 , 25 . Other library preparation and sequencing approaches which consider the sequence of the complementary strand, such as duplex sequences 15 , and circular consensus sequencing 26 , should improve sequence accuracy, although this would be at the expense of sequence efficiency.…”

Section: Discussionmentioning

confidence: 99%

A genome-wide mutation analysis method enabling high-throughput identification of chemical mutagen signatures

Matsumura

Fujita

Yamane

et al. 2018

Sci Rep

View full text Add to dashboard Cite

Trinucleotide mutational signatures extracted from cancer genomes provide clues useful in understanding the roles of mutagens and mutagenic mechanisms in cancer development. The lack of a simple method for genome-wide analysis of alterations induced by mutagens hampers the identification of trinucleotide signatures of mutagen exposure and evaluation of their relationships with human cancers. Here, we describe a novel approach to facilitate analysis of chemically induced mutations in bacterial cells by detection of increased frequencies of base substitutions after mutagen exposure, using paired-end overlapping next-generation sequencing. DNA samples from Salmonella typhimurium strain TA100, exposed to three alkylating agents, ethylnitrosourea (ENU), methylnitrosourea (MNU), and ethyl methansulphonate (EMS), were analysed. The G:C > A:T mutation frequency was increased in all samples, whereas A:T base pair substitution frequencies were increased specifically in samples exposed to ENU, consistent with previous reports. Mutation patterns in the context of 96 possible trinucleotide formats in these samples exhibited a sharp peak corresponding to an NpCpY consensus sequence, which is similar to the mutational signature of alkylating agents in human cancer. These results indicate that our approach can be useful in facilitating the understanding of mechanisms underlying chemical mutagenicity and for identification of unknown causal mutagens in human cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

A genome-wide mutation analysis method enabling high-throughput identification of chemical mutagen signatures

Matsumura

Fujita

Yamane

et al. 2018

Sci Rep

View full text Add to dashboard Cite

show abstract

Gene expression profile in BALB/c‐3T3 cells transformed with beryllium sulfate

Joseph

Muchnok

Ong

2001

Molecular Carcinogenesis

View full text Add to dashboard Cite

Differential gene expression was studied to understand the potential molecular mechanism responsible for cell transformation and tumorigenesis induced by beryllium. Cell lines were derived from tumors developed in nude mice injected subcutaneously with BALB/c-3T3 cells morphologically transformed with beryllium sulfate. Using the Atlas mouse 1.2 cDNA expression microarray, the expression profiles of 1176 genes, belonging to several different functional categories, were studied in the tumor cells as well as in the nontransformed control cells. Expression of 18 genes belonging to two functional groups was found to be consistently and reproducibly different (at least twofold) in the tumor cells compared with the control cells. The functional groups and the differentially expressed genes are as follows: The cancer-related genes (nine genes) were the ets-related transcription factor activated by ras, colony-stimulating factor, A-myb, sky, cot1, c-fos, c-jun, c-myc, and R-ras proto-oncogenes. The DNA synthesis, repair, and recombination genes (nine genes) were the DNA replication licensing factor MCM4, the DNA replication licensing factor MCM5, the DNA mismatch repair gene PMS2, the DNA excision repair gene, the DNA mismatch repair gene MSH2, the ultraviolet excision repair gene Rad23 DNA ligase 1, Rad51, and Rad52. The differential gene expression profile was confirmed with reverse transcription-polymerase chain reaction using primers specific for the differentially expressed genes. In general, expression of the cancer-related genes was upregulated, while expression of genes involved in DNA synthesis, repair, and recombination was downregulated in the tumor cells compared with the control cells. Using c-fos and c-jun, two of the differentially expressed genes, as model genes, we have found that in the nontransformed BALB/c-3T3 cells, the beryllium-induced transcriptional activation of these genes was dependent on pathways of protein kinase C and mitogen-activated protein kinase and independent of reactive oxygen species. These results indicate that beryllium-induced cell transformation and tumorigenesis are accompanied by and are possibly a product of alterations in expression of genes related to cancer and to DNA synthesis, repair, and recombination.

show abstract