# Kenneth D. Tartof
**Kenneth D. Tartof** is a molecular geneticist known for work on *Drosophila* genetics carried out at the Institute for Cancer Research, Fox Chase Cancer Center in Philadelphia. His research addressed three connected problems: how cells regulate the number of their ribosomal RNA genes, how heterochromatin (tightly packed, mostly gene-silencing form of DNA) silences genes moved next to it (position-effect variegation), and how a gene can sense the presence of its homologous copy on the other chromosome, a class of phenomena named trans-sensing effects.[1](https://www.annualreviews.org/content/journals/10.1146/annurev.ge.09.120175.002035) • [2](https://d.docksci.com/trans-sensing-effects-from-drosophila-to-humans_5f15a378097c47a0608b4569.html)
| Fact | Detail |
|---|---|
| Field | Molecular genetics of *Drosophila melanogaster*: rRNA gene regulation, heterochromatin, position-effect variegation[3](https://doi.org/10.1093/genetics/73.1.57) • [4](https://flybase.org/reports/FBrf0040503.html) |
| Training | PhD in Genetics, University of Michigan (Horace H. Rackham School of Graduate Studies), 1968[5](https://deepblue.lib.umich.edu/handle/2027.42/187882?show=full) |
| Career affiliation | The Institute for Cancer Research, Fox Chase Cancer Center, Philadelphia, from at least 1975[1](https://www.annualreviews.org/content/journals/10.1146/annurev.ge.09.120175.002035) |
| Signature work | "A structural basis for variegating position effects", *Cell*, 1984[4](https://flybase.org/reports/FBrf0040503.html) |
| Coined term | "Trans-sensing effects", proposed in a 1991 *Cell* minireview[2](https://d.docksci.com/trans-sensing-effects-from-drosophila-to-humans_5f15a378097c47a0608b4569.html) |
| Funding | National Institute of General Medical Sciences, National Cancer Institute, and National Center for Research Resources (NIH)[6](https://doi.org/10.1002/dvg.1020100306) |
| Legacy | PEV modifier genetics he helped develop underpins later work from HP1 and Su(var) genes to the human HUSH silencing complex[7](https://pmc.ncbi.nlm.nih.gov/articles/PMC4487827/) |
## Training and early career
Tartof received his PhD in Genetics in 1968 from the University of Michigan's Horace H. Rackham School of Graduate Studies, with a thesis titled *Gene Interaction in Drosophila Melanogaster: The Vermilion–Suppressor of Vermilion System*.[5](https://deepblue.lib.umich.edu/handle/2027.42/187882?show=full) According to his 1969 paper in *Genetics*, he extended this doctoral work on the regulation of tryptophan pyrrolase by the vermilion–suppressor of vermilion system.[8](https://academic.oup.com/genetics/article/62/4/781/5989400)
By 1975 he was at The Institute for Cancer Research, Fox Chase Cancer Center, Philadelphia, the affiliation printed on his review "Redundant Genes" in that year's *Annual Review of Genetics* (volume 9, pages 355–385).[1](https://www.annualreviews.org/content/journals/10.1146/annurev.ge.09.120175.002035) His variegation research at Fox Chase was funded by the National Institute of General Medical Sciences, the [National Cancer Institute](https://www.edgepedia.org/national-cancer-institute), and the National Center for Research Resources.[6](https://doi.org/10.1002/dvg.1020100306)
## Representative work
His 1984 *Cell* paper "A structural basis for variegating position effects" ([doi:10.1016/0092-8674(84)90422-7](https://doi.org/10.1016/0092-8674(84)90422-7)) gave a structural account of a classic variegating mutation. It showed that the euchromatic breakpoints of three variegating *white* mutants are clustered about 25 kb downstream of the *white* structural gene, that in each case the *white* locus is adjoined in the heterochromatin to a mobile genetic element rather than to satellite DNA, and that revertants of the mutant *wm4* are reinversions which leave the original *wm4*–heterochromatic junction intact, so some heterochromatin-derived sequences remain joined to *white* at its new location.[4](https://flybase.org/reports/FBrf0040503.html)
## Position-effect variegation and the boundary model
Position-effect variegation (PEV) occurs when a euchromatic gene is placed adjacent to centromeric heterochromatin or a telomeric domain, so the locus is active in some cells and silent in others.[9](https://staffpubs.fccc.edu/article/24295) Before the variegation work, Tartof had shown that the ribosomal RNA genes of *Drosophila* can undergo a disproportionate replication of their number, and that mutants partially deficient for rDNA can increase their rRNA gene number to the wild-type level and transmit this new genotype to successive generations.[3](https://doi.org/10.1093/genetics/73.1.57) According to his 1979 *Cell* paper, transcribed and spacer sequences of these rRNA genes evolve.[10](https://doi.org/10.1016/0092-8674(79)90268-x)
The 1984 molecular findings were developed in follow-up work. Cloning of the euchromatic–heterochromatic junctions of *wm4*, *wmMc*, and *wm51b* confirmed that the "heterochromatic" DNA immediately joined to *white* has the properties of mobile elements, and X-ray-induced revertants of *wm4* reinvert the *w*⁺ locus together with more than 3 kb of adjacent heterochromatic sequence, showing that the junction plus adjoining heterochromatin is not sufficient to variegate neighboring euchromatic loci.[11](https://doi.org/10.1093/genetics/120.1.181) A 1989 *Developmental Genetics* paper reported 12 dominant enhancers of variegation induced by P-element mutagenesis, representing four loci on the second and third chromosomes and falling into two reciprocally acting classes; it noted that in *Drosophila* 20–30 loci can dominantly modify variegation, and proposed a mass-action model in which class I genes code for proteins involved in assembling heterochromatic domains.[6](https://doi.org/10.1002/dvg.1020100306) Because the three *wm4* revertants carry some heterochromatically derived sequences with them upon restoration of the wild-type phenotype, Tartof proposed a boundary model: variegation is controlled not from a heterochromatic sequence immediately adjacent to the variegating gene but from some site more internal to the heterochromatic domain itself.[6](https://doi.org/10.1002/dvg.1020100306) In a *Development* paper he extended these studies to propose a simple mechanism of X-chromosome inactivation, a purpose for genomic imprinting, and a general means of regulating the developmental timing at which genes become heterochromatically repressed.[12](https://articles.researchsolutions.com/mechanisms-for-the-construction-and-developmental-control-of-heterochromatin-formation-and-imprinted-chromosome-domains/doi/10.1242/dev.108.supplement.35)
## Trans-sensing effects and their reception
A *Cell* minireview recommended retaining the older term "transvection" for somatic pairing effects closely resembling those originally described in earlier work, and drew on the zeste–white paradigm, in which paired copies of *w*⁺ give a lemon eye color in a *zeste* mutant background while rearrangements that disrupt pairing near *white* restore wild-type red color; homologous pairing of chromosomes in mitotic cells is well established in *Drosophila* and other dipteran insects.[2](https://d.docksci.com/trans-sensing-effects-from-drosophila-to-humans_5f15a378097c47a0608b4569.html)
Later reviews adopted the framework. A *Cell* review records that the term was introduced to encompass allelic pairing-dependent phenomena even when they have different underlying mechanisms, distinguishing transvection, a directional interaction between unlike mutant alleles, from pairing-dependent repression, a reciprocal interaction between like alleles. At the *brown* eye pigment locus, one copy is subject to cis-silencing when heterochromatin is juxtaposed nearby, an example of PEV, which in turn silences the homologous copy; *white* is insensitive to trans-inactivation in poorly paired heterozygotes but is trans-inactivated in well-paired heterozygotes.[13](https://www.cell.com/cell/fulltext/S0092-8674(00)81161-7) The 1984 *Cell* paper is also cited in specialist treatments of the genetics of chromatin assembly.[15](https://onlinelibrary.wiley.com/doi/10.1002/bies.950110105)
## References
1. K. D. Tartof, "Redundant Genes", *Annual Review of Genetics* 9:355–385 (1975). https://www.annualreviews.org/content/journals/10.1146/annurev.ge.09.120175.002035
2. "Trans-sensing effects from Drosophila to humans", *Cell* 65:201–203 (19 April 1991). https://d.docksci.com/trans-sensing-effects-from-drosophila-to-humans_5f15a378097c47a0608b4569.html
3. "Regulation of ribosomal RNA gene multiplicity in Drosophila melanogaster", *Genetics* 73(1):57 (1973). https://doi.org/10.1093/genetics/73.1.57
4. "A structural basis for variegating position effects", *Cell* 37:869–878 (1984), FlyBase record FBrf0040503. https://flybase.org/reports/FBrf0040503.html
5. K. D. Tartof, *Gene Interaction in Drosophila Melanogaster: The Vermilion–Suppressor of Vermilion System*, PhD thesis, University of Michigan, 1968. https://deepblue.lib.umich.edu/handle/2027.42/187882?show=full
6. "Towards an understanding of position effect variegation", *Developmental Genetics* (1989). https://doi.org/10.1002/dvg.1020100306
7. "Epigenetic silencing by the HUSH complex mediates position-effect variegation in human cells", *Science* (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4487827/
8. "Interacting Gene Systems: I. The Regulation of Tryptophan Pyrrolase by the Vermilion–Suppressor of Vermilion System in Drosophila", *Genetics* 62(4):781–795 (1969). https://academic.oup.com/genetics/article/62/4/781/5989400
9. Fox Chase Cancer Center faculty publications on position effect variegation. https://staffpubs.fccc.edu/article/24295
10. https://doi.org/10.1016/0092-8674(79)90268-x
11. "Dosage-dependent modifiers of position effect variegation in Drosophila and a mass action model that explains their effect", *Genetics* 120(1):181 (1988). https://doi.org/10.1093/genetics/120.1.181
12. "Mechanisms for the construction and developmental control of heterochromatin formation and imprinted chromosome domains", *Development* Supplement (1988). https://articles.researchsolutions.com/mechanisms-for-the-construction-and-developmental-control-of-heterochromatin-formation-and-imprinted-chromosome-domains/doi/10.1242/dev.108.supplement.35
13. https://www.cell.com/cell/fulltext/S0092-8674(00)81161-7
14. "Genomic imprinting and position-effect variegation in Drosophila melanogaster". https://pmc.ncbi.nlm.nih.gov/articles/PMC1460573/
15. "Position effect variegation in Drosophila: Towards a genetics of chromatin assembly", *BioEssays*. https://onlinelibrary.wiley.com/doi/10.1002/bies.950110105
16. https://www.cell.com/fulltext/S0092-8674(00)81159-9
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*Topic: Encyclopedia › Life and health › Life and health scientists › Life scientists › Researchers in genetics, genomics, and genome engineering › Epigenetics and chromatin biology*
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