Group Leader:
Iain Hagan
After completing my PhD studies I went to Japan on a 4-year postdoctoral fellowship with Professor Mitsuhiro Yanagida in Kyoto University. I returned to the UK in 1993 with a Cancer Research Campaign Return Fellowship to establish a group in The University of Manchester. I continued to work in what later became the Faculty of Life Sciences at The University of Manchester, with further Cancer Research Campaign Fellowship support before moving to the Paterson Institute for Cancer Research in 2001. In 1999 I was awarded the Human Frontier Science Program 10th Anniversary Medal and in 2001 was the recipient of the BSCB Hooke Medal. I am currently a Senior Group Leader at the Paterson Institute for Cancer Research.
Postdoctoral Fellows
Marisa Alonso Nuñez
Marisa Madrid
Associate Scientist
Agnes Grallert
Graduate Students
Dorota Feret
Avinash Patel
Elvan Boke
Yisu Wang
Cell Division Group - Cut 12
Rachel Bartlett found the cut12.1 mutant in the original dip screen in the Paul Nurse's lab (Broek et al., 1991). Immunofluorescence staining to localise microtubules, chromosomes and the spindle pole antigen Sad1 showed that the cells block progression through mitosis due to a defect in the formation of the mitotic spindle. Microtubules appeared to extend from a single point in to give a Y or V shaped pattern. Sad1 was often found at this point, however it was much fainter than at a second point that rarely nucleated microtubules. Thus in this mutation one SPB worked while one failed.
Cloning and characterisation of cut12+ showed that it encoded a spindle pole component that sequence did not resemble any sequences in the database at the time (Bridge et al., 1998). They also established that the cut12+ gene was identical to the stf1+ gene which had been identified and characterised by Young and Hudson (Hudson et al., 1991; Hudson et al., 1990). Young and Hudson had identified stf1 mutants because these mutations enabled cdc25.22 cells to grow at the restrictive temperature (Hudson et al., 1990). The synthetic interaction between cdc25.22 and the recessive cut12.1 mutation (Bridge et al., 1998) suggests that the cut12.1 phenotype may actually arise from defective commitment to mitosis rather than from a requirement in microtubule nucleation per se. Subsequent work established that Cut12 recruits Plo1 to the SPB and so regulates mitotic commitment.
references
Bridge, A. J., Morphew, M., Bartlett, R., and Hagan, I. M. (1998). The fission yeast SPB component Cut12 links bipolar spindle formation to mitotic control. Genes and Development 12, 927-942.
Broek, D., Bartlett, R., Crawford, K., and Nurse, P. (1991). Involvement of p34cdc2 in establishing the dependency of S-phase on mitosis. Nature 349, 388-393.
Hudson, J. D., Feilotter, H., Lingner, C., Rowley, R., and Young, P. (1991). stf1; a new supressor of the mitotic control gene cdc25 in Schizoszcchzromyces pombe. Cold Spring Harbor Symposia on Quantitative Biology 56, 599-604.
Hudson, J. D., Feilotter, H., and Young, P. G. (1990). stf1: non wee mutations epistatic to cdc25 in the fission yeast Schizosaccharomyces pombe. Genetics 126, 309-315.