McKim, KS, Howell AM, Rose AM.  1988.  The effects of translocations on recombination frequency in Caenorhabditis elegans. Genetics. 120:987-1001.
McKim, KS, Rose AM.  1990.  Chromosome I duplications in Caenorhabditis elegans. Genetics. 124:115-32.Website
McKim, KS, Jang JK, Theurkauf WE, Hawley RS.  1993.  Mechanical basis of meiotic metaphase arrest. Nature. 362:364-366.
Hawley, RS, McKim KS, Arbel T.  1993.  Meiotic segregation in Drosophila melanogasterfemales: molecules, mechanisms and myths. Ann. Rev. Genet.. 27:281-317.
Hawley, RS, Irick HA, Zitron AE, Haddox DA, Lohe AR, New C, Whitley MD, Arbel T, Jang JK, McKim KS et al..  1993.  There are two mechanisms of achiasmate segregation in Drosophila females, one of which requires heterochromatic homology. Developmental Genetics. 13:440-467.
McKim, KS, Peters K, Rose AM.  1993.  Two types of sites required for meiotic chromosome pairing in Caenorhabditis elegans. Genetics. 134:749-768.
McKim, KS, Rose AM.  1994.  Spontaneous duplication loss and breakage in Caenorhabditis elegans. Genome. 37:595-606.Website
Hari, KL, Santerre A, Sekelsky JJ, McKim KS, Boyd JB, Hawley RS.  1995.  The mei-41 gene of D. melanogaster is a structural and function homolog of the human ataxia telangiectasia gene. Cell. 82:815-821.
McKim, KS, Hawley RS.  1995.  Chromosomal control of meiotic cell division. Science. 270:1595-1601.
Sekelsky, JJ, McKim KS, Chin GM, Hawley RS.  1995.  The Drosophila meiotic recombination gene mei-9 encodes a homologue of the yeast excision repair protein Rad1. Genetics. 141:619-627.
McKim, KS, Hayashi-Hagihara A.  1998.  mei-W68 in Drosophila melanogaster encodes a Spo11 homolog: evidence that the mechanism for initiating meiotic recombination is conserved. Genes & Dev.. 12:2932-42. AbstractWebsite
Meiotic recombination requires the action of several gene products in both Saccharomyces cerevisiae and Drosophila melanogaster. Genetic studies in D. melanogaster have shown that the mei-W68 gene is required for all meiotic gene conversion and crossing-over. We cloned mei-W68 using a new genetic mapping method in which P elements are used to promote crossing-over at their insertion sites. This resulted in the high-resolution mapping of mei-W68 to a 18-kb region that contains a homolog of the S. cerevisiae spo11 gene. Molecular analysis of several mutants confirmed that mei-W68 encodes an spo11 homolog. Spo11 and MEI- W68 are members of a family of proteins similar to a novel type II topoisomerase. On the basis of this and other lines of evidence, Spo11 has been proposed to be the enzymatic activity that creates the double- strand breaks needed to initiate meiotic recombination. This raises the possibility that recombination in Drosophila is also initiated by double-strand breaks. Although these homologous genes are required absolutely for recombination in both species, their roles differ in other respects. In contrast to spo11, mei-W68 is not required for synaptonemal complex formation and does have a mitotic role.
McKim, KS, Green-Marroquin BL, Sekelsky JJ, Chin G, Steinberg C, Khodosh R, Hawley RS.  1998.  Meiotic synapsis in the absence of recombination. Science. 279:876-878.
Sekelsky, JJ, McKim KS, Messina L, French RL, Hurley WD, Arbel T, Chin GM, Deneen B, Force SJ, Hari KL et al..  1999.  Identification of novel Drosophila meiotic genes recovered in a P- element screen. Genetics. 152:529-42. AbstractWebsite
The segregation of homologous chromosomes from one another is the essence of meiosis. In many organisms, accurate segregation is ensured by the formation of chiasmata resulting from crossing over. Drosophila melanogaster females use this type of recombination-based system, but they also have mechanisms for segregating achiasmate chromosomes with high fidelity. We describe a P-element mutagenesis and screen in a sensitized genetic background to detect mutations that impair meiotic chromosome pairing, recombination, or segregation. Our screen identified two new recombination-deficient mutations: mei-P22, which fully eliminates meiotic recombination, and mei-P26, which decreases meiotic exchange by 70% in a polar fashion. We also recovered an unusual allele of the ncd gene, whose wild-type product is required for proper structure and function of the meiotic spindle. However, the screen yielded primarily mutants specifically defective in the segregation of achiasmate chromosomes. Although most of these are alleles of previously undescribed genes, five were in the known genes alphaTubulin67C, CycE, push, and Trl. The five mutations in known genes produce novel phenotypes for those genes.
McKim, KS, Jang JK, Sekelsky JJ, Laurencon A, Hawley RS.  2000.  mei-41 is required for precocious anaphase in Drosophila females. Chromosoma. 109:44-49.
Page, SL, McKim KS, Deneen B, Van Hook TL, Hawley RS.  2000.  Genetic studies of mei-P26 reveal a link between the processes that control germ cell proliferation in both sexes and those that control meiotic exchange in Drosophila. Genetics. 155:1757-72.. AbstractWebsite
We present the cloning and characterization of mei-P26, a novel P- element-induced exchange-defective female meiotic mutant in Drosophila melanogaster. Meiotic exchange in females homozygous for mei-P26(1) is reduced in a polar fashion, such that distal chromosomal regions are the most severely affected. Additional alleles generated by duplication of the P element reveal that mei-P26 is also necessary for germline differentiation in both females and males. To further assess the role of mei-P26 in germline differentiation, we tested double mutant combinations of mei-P26 and bag-of-marbles (bam), a gene necessary for the control of germline differentiation and proliferation in both sexes. A null mutation at the bam locus was found to act as a dominant enhancer of mei-P26 in both males and females. Interestingly, meiotic exchange in mei-P26(1); bam(Delta)(86)/+ females is also severely decreased in comparison to mei-P26(1) homozygotes, indicating that bam affects the meiotic phenotype as well. These data suggest that the pathways controlling germline differentiation and meiotic exchange are related and that factors involved in the mitotic divisions of the germline may regulate meiotic recombination.
Liu, H, Jang JK, Graham J, Nycz K, McKim KS.  2000.  Two genes required for meiotic recombination in Drosophila are expressed from a dicistronic message. Genetics. 154:1735-46. AbstractWebsite
We have isolated two alleles of a previously unidentified meiotic recombination gene, mei-217. Genetic analysis of these mutants shows that mei-217 is a typical "precondition" gene. The phenotypes of the mutants are meiosis specific. The strongest allele has 10% of the normal level of crossing over, and the residual events are distributed abnormally. We have used double mutant analysis to position mei-217 in the meiotic recombination pathway. In general, mutations causing defects in the initiation of meiotic recombination are epistatic to mutations in mei-41 and spnB. These two mutations, however, are epistatic to mei-217, suggesting that recombination is initiated normally in mei-217 mutants. It is likely that mei-217 mutants are able to make Holliday junction intermediates but are defective in the production of crossovers. These phenotypes are most similar to mutants of the mei-218 gene. This is striking because mei-217 and mei-218 are part of the same transcription unit and are most likely produced from a dicistronic message.
Giunta, KL, Jang JK, Manheim EM, Subramanian G, McKim KS.  2002.  subito encodes a kinesin-like protein required for meiotic spindle pole formation in Drosophila melanogaster. Genetics. 160:1489-1501.
Manheim, EA, Jang JK, Dominic D, McKim KS.  2002.  Cytoplasmic localization and evolutionary conservation of MEI-218, a protein required for meiotic crossing over in Drosophila. Mol. Biol. Cell. 13:84-95.
McKim, KS, Jang JK, Manheim EA.  2002.  Meiotic recombination and chromosome segregation in Drosophila females. Annu. Rev. Genet.. 36:205-232.
Jang, JK, Sherizen DE, Bhagat R, Manheim EA, McKim KS.  2003.  Relationship of DNA double-strand breaks to synapsis in Drosophila. J. Cell. Sci.. 116:3069-3077.
Bhagat, R, Manheim EA, Sherizen DE, McKim KS.  2004.  Studies on crossover specific mutants and the distribution of crossing over in Drosophila females. Cytogenetic and Genome Res.. 107:160-71.