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Biomedical subjects

E J Foss

Publications and source records attributed to E J Foss.

4 recordsLinked to original sources
PubMed2001

Tof1p regulates DNA damage responses during S phase in Saccharomyces cerevisiae.

A tof1 mutant was recovered in a screen aimed at identifying genes involved specifically in the S phase branch of the MEC1-dependent DNA damage response pathway. The screen was based on the observation that mutants missing this branch are particularly dependent on the cell cycle-wide branch and, therefore, on RAD9, for surviving DNA damage. tof1 and rad9 conferred synergistic sensitivity to MMS, UV, and HU, and the double mutant was incapable of slowing S phase in response to MMS, inducing RNR3 transcription in response to UV, and phosphorylating Rad53p in response to HU. TOF1's contribution to DNA damage response appeared to be restricted to S phase, since TOF1 did not contribute to UV-induced transcription during G1 or to the cdc13-1-induced block to anaphase in G2/M. I suggest a model in which Tof1p functions to link Mec1p with Rad53p.

Cell Cycle Proteins↗
PubMed1995

A test of a counting model for chiasma interference.

According to the model of FOSS, LANDE, STAHL and STEINBERG, chiasma interference is a reflection of the requirement for crossovers to be separated by an organism-specific number of potential conversion events without associated crossovers. This model predicts that tetrads with close double crossovers should be enriched for conversion events that themselves are not associated with crossing over. We tested this prediction in Saccharomyces cerevisiae and found it to be unfulfilled.

Chromatids↗
PubMed1991

Specificity of repeat-induced point mutation (RIP) in Neurospora: sensitivity of non-Neurospora sequences, a natural diverged tandem duplication, and unique DNA adjacent to a duplicated region.

The process designated RIP (repeat-induced point mutation) alters duplicated DNA sequences in the sexual cycle of Neurospora crassa. We tested whether non-Neurospora sequences are susceptible to RIP, explored the basis for the observed immunity to this process of a diverged tandem duplication that probably arose by a natural duplication followed by RIP (the Neurospora zeta-eta region), and investigated whether RIP extends at all into unique sequences bordering a duplicated region. Bacterial sequences of the plasmid pUC8 and of a gene conferring resistance to hygromycin B were sensitive to RIP in N. crassa when repeated in the genome. When the entire 1.6-kb zeta-eta region was duplicated, it was susceptible to RIP, but was affected by it to a lesser extent than other duplications. Only three of 62 progeny from crosses harboring unlinked duplications of the region showed evidence of changes. We attribute the low level of alterations to depletion of mutable sites. The stability of the zeta-eta region in strains having single copies of the region suggests that the 14% divergence of the tandem elements is sufficient to prevent RIP. DNA sequence analysis of unduplicated pUC8 sequences adjacent to a duplication revealed that RIP continued at least 180 bp beyond the boundary of the duplication. Three mutations occurred in the 200-bp segment of bordering sequences examined.

Base Sequence↗