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Book Reviews

Genomes, 2nd edition

T. A. Brown, Editor.

BIOS Scientific Publishers, Oxford, U.K. 2002. 572 pp.

An emerging challenge in the current era of whole genome

projects is to integrate these complex data sets with existing

knowledge in biological disciplines ranging from medical

genetics to evolutionary biology. The second edition of

Genomes is a bold attempt to convey the impact these genome

projects have had and will continue to have on biological

research. It bridges the gap between basic textbooks and

emerging data in the scientific literature and distills this

information in a way that is readily accessible to students and

educators alike.

The major strengths of Genomes lies in its unique organi-

zation. It is divided into four parts that proceed through

a logical and intuitive progression of discussions concerning

transcriptosomes and proteomes, genomic technologies and

analytical techniques, genome function, and how genomes

replicate and evolve. All chapters are well organized and

provide supplementary material that is important for those

wishing to explore the subject matter in greater depth. The

''Learning Outcomes,'' ''Study Aids,'' and ''Questions'' sec-

tions that accompany each chapter assist the students and

instructors to set appropriate goals upon which to focus their

efforts. The ''Further Reading'' section is especially valuable

in highlighting recent reviews on subject matter that may

warrant further attention.

Brown does an admirable job of describing newly

emerging technologies that have helped shape genomic bi-

ology. Nevertheless, several minor errors in the text were

present in discussions regarding DNA microarray technol-

ogy. For example, it would be more correct to state that

phosphoramidite-based chemistry, instead of modified

dNTPs, is commonly used in the chemical synthesis of

high-density oligonucleotide microarrays. Likewise, the de-

sign and application of DNA microarrays that can survey the

expression of many thousands of genes was not sufficiently

emphasized. Future editions may also benefit from discuss-

ing use of DNA microarray technology to classify different

diseases, such as various kinds of cancer.

Genomes is enhanced by beautiful color figures that help

432

convey complex information and enhance the natural flow of

the well-written text. The structures of nucleic acid binding

proteins such as histones, transcription factors, and RNA

polymerases were especially important in adding intellectual

rigor while bringing the text to life. At times, some of the

more simple diagrammatic figures may have been over-used

and distracting to the reader. However, in general, they

provide a useful resource for students to clarify what is stated

in the text.

Overall, Genomes is successful in keeping up with the

rapidly changing and dynamic world of genomic biology.

Contrary to what is stated in the Appendix, it is not written

on a level roughly equivalent to review articles appearing in

professional journals such as Trends in Genetics and Nature.

However, it is well suited to be a textbook in beginning and

mid-level undergraduate courses in molecular or genomic

biology or a supplement for more advanced undergraduate

courses. It provides the basic information necessary to take

the next step towards having an in depth understanding the

professional literature. Due to the current state of genomic

biology, it is likely that the content of certain chapters will

need to be modified in the near future. Therefore, we

eagerly look forward to future editions of this wonderful

textbook.

MAZEN W. KARAMAN

JOSEPH G. HACIA

Department of Biochemistry and Molecular Biology

Keck School of Medicine

University of Southern California

2250 Alcazar Street, IGM 240

Los Angeles, CA 91101

DOI: 10.1093/jhered/esg082

Book Reviews

433

... Under normal physiological conditions, the DNA repair mechanism is activated in response to DNA damage in an attempt to correct the defected DNA and restore normal cell function [2]. This is crucial to cell cycle as it ensures that any genetic mutations are corrected before mitosis and not passed onto daughter cells [3]. Hematological malignancies (HM) account for approximately 10% of all newly diagnosed cancers and are usually characterized by genetic defect in the form of chromosomal translocation or breakpoint/fusion [4]. ...

DNA repair plays an essential role in protecting cells that are repeatedly exposed to endogenous or exogenous insults that can induce varying degrees of DNA damage. Any defect in DNA repair mechanisms results in multiple genomic changes that ultimately may result in mutation, tumor growth, and/or cell apoptosis. Furthermore, impaired repair mechanisms can also lead to genomic instability, which can initiate tumorigenesis and development of hematological malignancy. This review discusses recent findings and highlights the importance of DNA repair components and the impact of their aberrations on hematological malignancies.

... The discrepancy likely results from the limitation of whole-genome shotgun sequencing, an older platform that acquires contiguous sequence data of large genomes and that involves genome assembly by finding overlapping fragments. It has several limitations, such as a time-consuming process, errors in genome alignment, and the challenge of assembling repetitive sequences in genomes (Karaman, 2003). Currently, NGS technology has been used for a broad range of applications due to the improvement of accuracy and sensitivity and has significantly facilitated the scope of genetic research (Metzker, 2010). ...

Shiga toxin-producing Escherichia coli (STEC) is a notorious foodborne pathogen containing stx genes located in the sequence region of Shiga toxin (Stx) prophages. Stx prophages, as one of the mobile elements, are involved in the transfer of virulence genes to other strains. However, little is known about the diversity of prophages among STEC strains. The objectives of this study were to predict various prophages from different STEC genomes and to evaluate the effect of different stress factors on Stx prophage induction. Forty bacterial whole-genome sequences of STEC strains obtained from National Center for Biotechnology Information (NCBI) were used for the prophage prediction using PHASTER webserver. Eight of the STEC strains from different serotypes were subsequently selected to quantify the induction of Stx prophages by various treatments, including antibiotics, temperature, irradiation, and antimicrobial agents. After induction, Stx1-converting phage Lys8385Vzw and Stx2-converting phage Lys12581Vzw were isolated and further confirmed for the presence of stx genes using conventional PCR. Phage morphology was observed by transmission electron microscopy. The prediction results showed an average of 8–22 prophages, with one or more encoding stx, were predicted from each STEC genome obtained in this study. Additionally, the phylogenetic analysis revealed high genetic diversity of Stx prophages among the 40 STEC genomes. However, the sequences of Stx prophages in the genomes of STEC O45, O111, and O121 strains, in general, shared higher genetic homology than those in other serotypes. Interestingly, most STEC strains with two or more stx genes carried at least one each of Stx1 and Stx2 prophages. The induction results indicated EDTA and UV were the most effective inducers of Stx1 and Stx2 prophages of the 8 selected STECs, respectively. Additionally, both Stx-converting phages could infect non-pathogenic E. coli (WG5, DH5α, and MG1655) and form new lysogens. The findings of this study confirm that Stx prophages can be induced by environmental stress, such as exposure to solar radiation, and lysogenize other commensal E. coli strains.

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