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Indiana University Bloomington

Department of Biology

Faculty & Research

Faculty Profile

Carol Anderson

Photo of Carol Anderson
Research Images
Research photo by Carol Anderson

Spread meiotic yeast chromosomes. Green: Zip3 foci marking future crossovers. Red: Synaptonemal complex protein Zip1. Blue: DNA.

Research photo by Carol Anderson

Meiotic double-strand breaks (DSBs) are deliberately induced by the Spo11 enzyme; some become marked by ZMM foci and become crossovers. Remaining DSBs tend to become noncrossovers. How crossover sites are selected and how ZMM foci form are unknown.

Research photo by Carol Anderson

Yeast chromosome IX analyzed by Rec-seq. The four rows represent four progeny of a single meiosis. Red and blue lines indicate positions genotyped by sequencing. Red indicates the sequence matches Parent 1 and blue indicates Parent 2. Arrows indicate examples of crossovers and noncrossovers. Sites with a reciprocal genotype change in two progeny are crossovers; sites with non-reciprocal changes are noncrossovers.

Assistant Professor of Biology
Contact Information
By telephone: 812-856-5603, 6-9901(lab)
By fax: lab phone - 6-9901
JH 333

Anderson Lab Website

Program
Genome, Cell & Developmental Biology
Research Areas
  • Chromatin, Chromosomes, and Genome Integrity
  • Eukaryotic Cell Biology, Cytoskeleton and Signaling
  • Genomics and Bioinformatics
Education

Ph.D., University of California, San Francisco, 2008
Postdoctoral Fellow, University of California, San Francisco, 2009-2015

Awards

DeLill Nasser Award for Professional Development in Genetics, Genetics Society of America, 2015
Monique Braude Fellowship, Graduate Women in Science, 2014

Research Description

Homologous recombination is a critical DNA repair mechanism in all organisms. During recombination, damaged sections of DNA are replaced by replication of a homologous template, typically leading to precise restoration of the original sequence. When recombination is compromised, cells are forced to rely on more error-prone repair pathways, with potentially severe consequences such as cell death and carcinogenesis. Recombination is also a central feature of meiosis, creating the crossovers necessary for correct chromosome segregation and production of viable gametes. Since its discovery over a century ago, many of the mechanisms of recombination have been elucidated, but fundamental questions remain unanswered. My lab is studying these questions using meiosis in the budding yeast Saccharomyces cerevisiae as a model. We use a variety of approaches, including high-resolution fluorescence microscopy, whole-genome sequencing, classical genetics, and biochemistry.

Choice of crossover vs. noncrossover repair pathway

During meiosis, cells deliberately create double-strand DNA breaks as the opening act in a dramatic series of events in which pairs of chromosomes find each other, exchange segments via recombination, and undergo two successive rounds of division. The product of recombination can be a crossover, which is a reciprocal exchange of chromosome arms, or a noncrossover, a nonreciprocal exchange. Only crossovers help ensure proper chromosome segregation in meiosis, so germ cells intricately regulate recombination to ensure that a sufficient number of crossovers is made. This is very different from the situation in somatic cells, where recombination rarely produces crossovers. How do meiotic and mitotic cells create such strikingly different recombination outcomes? One answer involves a group of meiosis-specific proteins called the ZMMs (Zip2-Zip3-Zip4-Spo16, Msh4-Msh5, Mer3), which are found in most sexually reproducing organisms. These proteins form foci specifically at the meiotic double-strand breaks that will go on to become crossovers, while noncrossovers are not marked by such foci. ZMMs promote crossing over, but how they do so is not well understood. A major interest of my lab is understanding the function of the ZMM proteins – how and why they are recruited to some DSBs and not others, and how they promote crossing over.

Spatial patterning of recombination

A fascinating feature of meiotic crossovers is that they tend to be evenly spaced along chromosomes. This is known as interference, i.e. a crossover "interferes with" additional crossovers nearby. The mechanisms behind this self-organizing patterning process remain enigmatic. We are using a novel next-generation sequencing-based approach called Rec-seq to study interference and other aspects of the recombination landscape. We mate two yeast strains with thousands of single-nucleotide polymorphisms throughout their genomes, isolate haploid progeny by tetrad dissection, and genotype them by next-generation sequencing. The high-resolution, genome-wide picture of recombination provided by Rec-seq allows us to probe the mechanisms by which cells regulate the number and spacing of recombination sites.

Select Publications
Anderson CM, Oke A, Yam P, Zhuge T, Fung J. (2015) Reduced crossover interference and increased ZMM-independent recombination in the absence of Tel1/ATM.  PloS Genet. 11(8): e1005478.  [article]
Oke A, Anderson CM, Yam P, Fung JC. (2014) Controlling meiotic recombinational repair – specifying the roles of ZMMs, Sgs1 and Mms4 in crossover formation. PloS Genet. 10(10): e1004690.  [article]
Anderson CM, Chen SY, Dimon MT, Oke A, DeRisi JL, Fung JC. (2011) ReCombine: a suite of programs for detection and analysis of meiotic recombination in whole-genome datasets. PLoS One. 6(10):e25509.  [article]

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