Spring 2006 NEWS:  

We are back to our traditional time and location: M 10:00-12:00 LSA1022

For students: Please register with CRN 82693

The format is journal club. PDF files of the paper(s) to be discussed will be emailed and posted here.

April 10 Kowalczykowski lab

Jason Bell: Mediator proteins in recombination

April 24 Baldwin lab

Enoch Baldwin:

ABSTRACT
The dimeric Mus81/XPF structure-specific endonucleases contain helicase, DNA binding and nuclease domains and cleave non-canonical and branched DNA structures that arise during replication, recombination and nucleotide excision repair (NER). Deficiencies corrolate with DNA damage sensitivity, cancer predisposition, short lifespan and neurological disfunction and are associated with the human heritable disease Xeroderma pigmentosum. The heterodimeric human Mus81/XPF homolog XPF-ERCC1 (1) cleaves damaged DNA strand on the 5' side of nucleotide lesions or interstrand crosslinks in NER, completing the excision of the 24-32 nucleotide damage-containing ssDNA fragment initiated by XPG nuclease cleavage 3' to the lesion site. Key structure-functional questions are 1) how does the 3-D arrangement of protein domains allow for initiation and unwinding of the damaged DNA segment and 2) what accounts for its particular DNA specificity and junction-binding polarity. The Ellenberger lab recently published the structure of truncated hXPF-ERCC1 lacking the helicase domain which revealed the relative positions of nuclease and ssDNA binding surfaces. Utilizing the structure of an intact archael XPF helicase from the Ishino and co-workers (2), they construct of model of full-length XPF-ERCC1 bound to branched DNA which is consistent with known biochemical data. The structural similarity of ERCC1 to archael XPF/Mus81 nuclease domains, despite low sequence identity, suggests that this model will be generally informative for this class of proteins.

(1) Proc. Natl. Acad. Sci. 102, 11236-11241 (2005)

"Crystal structure and DNA binding functions of ERCC1, a subunit of the DNA structure-specific endonuclease XPF-ERCC1"

Oleg V. Tsodikov, Jacquelin H. Enzlin, Orlando D. Scharer, and Tom Ellenberger [pdf]

(2) Structure 13, 143-153 (2005)

"Crystal Structure and Functional Implications of Pyrococcus furiosus Hef Helicase Domain Involved in Branched DNA Processing"

Tatsuya Nishino, Kayoko Komori, Daisuke Tsuchiya, Yoshizumi Ishino [pdf]

May 8 Hunter lab

Kseniya Zakharyevich

"Mismatch Repair Proteins in Meiosis: Role of Exo1 in promoting crossing over".

1) Meiotic recombination intermediates and mismatch repair proteins
E.R. Hoffmann and R.H. Borts 2004 [pdf]

2) Exo1 Roles for Repair of DNA Double-Strand Breaks and Meiotic Crossing Over in Saccharomyces cerevisiae
Hideo Tsubouchi and Hideyuki Ogawa 2000 [pdf]

3) Inactivation of Exonuclease 1 in mice results in DNA mismatch repair defects, increased cancer susceptibility, and male and female sterility
Kaichun Wei, Alan B. Clark, Edmund Wong, Michael F. Kane, Dan J. Mazur, Tchaiko Parris, Nadine K. Kolas, Robert Russell, Harry Hou Jr., Burkhard Kneitz, Guohze Yang, Thomas A. Kunkel, Richard D. Kolodner, Paula E. Cohen, and Winfried Edelmann 2003 [pdf]

4) Decreased Meiotic Intergenic Recombination and Increased Meiosis I Nondisjunction in exo1 Mutants of Saccharomyces cerevisiae
David T. Kirkpatrick, John R. Ferguson, Thomas D. Petes and Lorraine S. Symington 2000 [pdf]

5) EXO1 and MSH4 differentially affect crossing-over and segregation
Kamal A. Khazanehdari, Rhona H. Borts 2000 [pdf]

May 22 Segal lab

David Segal is a new faculty member in the UC Davis Genome Center. His research focuses on gene targeting techniques.

"Better living through targeted recombination"

Our lab is designing chimeric nucleases to simulate targeted homologous
recombination for use in gene therapy and transgenic animals. The nucleases
are based on custom zinc finger DNA-binding proteins, which we can engineer
to bind specifically to a wide variety of DNA sequences. I will describe the
history of engineered zinc finger proteins and chimeric nucleases,
highlighting efforts in our lab to improve the technology and repair

endogenous genes.

David J. Segal, Ph.D.
UC Davis Genome Center
Dept Med Pharmacology
4513 GBSF
451 E. Health Sciences Dr.
Davis, CA 95616

Tel: 530-754-9134

Fax: 530-754-9658

Email: djsegal@ucdavis.edu

Web: www.genomecenter.ucdavis.edu/segal/

June 5 Wolf Heyer/Neil Hunter/Stephen Kowalczykowski

2006 Seillac Meeting Review

WINTER 2006 NEWS:  

We are back to our traditional time and location: M 10:00-12:00 LSA1022

For students: Please register with CRN 63155

The format is journal club. PDF files of the paper(s) to be discussed will be emailed and posted here.

January 9 Ken Burtis:

Recent discoveries have shed new light on mechanisms of interstrand crosslink repair. Focusing on the paper by Meetei et al. [pdf] and the review by Larry Thompson [pdf], I will discuss these discoveries in the context of my lab's work on crosslink repair in Drosophila.

January 23 Kowalczykowski lab

Amitabh Nimonkar: 'The art of making a D-loop'

No assignd reading.

February 6 Baldwin lab: cancelled

February 27 John Roth

"A role for selection in multi-step chromosome rearrangement"

Suggested reading: Roth et al. 2006 in press

Monday, March 6th, 10:00 -11:00, rm 1022 Life Sciences

Dr. Hisaji Maki, Professor of Molecular Biology

Nara Instititue of Technology

"Abnormality in the initiation DNA replication is monitored by highly repetitive rDNA array on chromosome XII in budding yeast".

We have previously shown that the temperature-sensitive phenotype of orc1-4 and orc2-1 mutants requires a programmed action of RAD9-dependent DNA damage checkpoint response at the restrictive temperatures. The findings also indicated that perturbation of origin-firing in chromosome replication causes some DNA lesion and triggers the checkpoint control, which ensures genomic integrity by stopping the cell cycle progress until lesion repaired or by inducing cell death when the lesion is not properly repaired. Here we show that in the orc mutants, DNA lesions were induced much more quickly and frequently within the ribosomal RNA gene (rDNA) locus than other chromosomal loci upon the temperature shift. orc mutant cells with an extensively reduced copy number of rDNA array gained growth at the restrictive temperatures, and the checkpoint response became faint in the cells after the temperature shift. In orc2-1 cells, completion of chromosomal duplication was delayed specifically to chromosome XII where the rDNA array is located, and the delay was partially suppressed when the rDNA copy number was reduced. These results suggest that the rDNA locus plays a role in monitoring abnormal initiation program of chromosomal replication and that the copy number of rDNA array modulates sensitivity of the monitoring.

March 13 Britt lab

Neil Huefner

Alternative mechanisms of NHEJ: What enzymes act to rejoin double strand

break products? Discussion will focus on the paper by Wang et.al. [pdf] and the

review by Bonatto et.al. [pdf], as well as work from our own lab.

FALL 2005 NEWS:  

Please note new time and location: 148 Briggs Hall F 10:30-12:30

For students: Please register with CRN42443

The format is journal club. PDF files of the paper(s) to be discussed will be emailed and posted here.

September 30 Kowalczykowski lab

Yun Wu

Osman et al. (2005) The F-Box DNA helicase Fbh1 Prevents Rhp51-dependent recombination without mediator proteins. MCB 25: 8084. [pdf]

October 14 Heyer lab

Xuan Li

Van Loock et al. (2003) ATP-mediated conformational changes in the RecA filament. Structure 11: 187. [pdf]

October 28 Hunter lab

Steve Oh

"Roles of the Sgs1 DNA Helicase During Meiotic Recombination"

November 18 Engebrecht lab

Note: We will meet in SLB2064 Friday 11/18 10:30-12:30 pm.

Eleanor M. Maine, Jessica Hauth, Thomas Ratliff, Valarie E. Vought, Xingyu She1 and William G. Kelly. EGO-1, a Putative RNA-Dependent RNA Polymerase, Is Required for Heterochromatin Assembly on Unpaired DNA during C. elegans Meiosis. Curr. Biol. 15, 1972-1978 [pdf]

December 2 Burgess lab

Sean Burgess

Hochwagen A, Tham WH, Brar GA, Amon A. The FK506 binding protein Fpr3 counteracts protein phosphatase 1 to maintain meiotic recombination checkpoint activity. Cell. 2005 Sep 23;122(6):861-73. [pdf]

The winter quarter will feature the following labs: Britt, Baldwin, Roth, Burtis. I hope to return to the traditional M 10-12 slot in LSA1022.