Dr Stephen Gregory
|Org Unit||Genetics & Evolution|
|Telephone||+61 8 8313 7536|
Molecular Life Sciences
The aim of our research is to understand the genetic control of cell division, using the most powerful model system available, Drosophila melanogaster. Drosophila has the great advantages of a completely sequenced and annotated genome, an existing detailed description of its development at the cellular level and the availability of mutants for most genes. In addition, it is a convenient system for sophisticated molecular, genetic and cell biological techniques, allowing us to probe cellular and developmental processes. Drosophila therefore provides the most exciting intellectual challenges in studying developmental biology, because so many experimental approaches are possible. Experience has shown that discoveries made in Drosophila often lead the way by explaining mechanisms or providing tools that help the analysis of cell and developmental biology in other organisms.
Our work has identified key genes that control cell division and allowed us to see what they are doing in their normal setting: a live, developing animal. We are currently working towards being able to visualise the cellular machinery that divides cells in two at the end of mitosis, and to find the genes that regulate this process. This work is critical for an understanding of how normal growth works, but also to give us potential therapeutics that will allow us to block the uncontrolled cell division seen in cancer.
Cancers are cells that not only divide too much, but also usually divide unstably, gaining and losing chromosomes. This chromosomal instablility is not seen in normal dividing cells, so it may be an ideal chemotherapy target - something that we can affect in the cancer without hurting normal cells.
Using the advantages of Drosophila genetics, we have screened for gene knockouts that can kill unstably dividing cells, but not normal ones. We have found several ways to specifically kill cells with chromosomal instability, including targeting the JNK pathway, centrosomes or cell metabolism. We are now working to explain why unstably dividing cells are sensitive to these processes, and how we can best target them.
Z. Shaukat, D.Liu, R. Hussain, M. Khan and S. L. Gregory (2015). The role of JNK signaling in responses to oxidative DNA damage.
Current Drug Targets (in press) Impact 3.9 Citations: 2
D. Liu, Z. Shaukat, R. Hussain, M. Khan and S. L. Gregory (2015). Drosophila as a model for chromosomal instability.
AIMS Genetics 2:1-12
Z. Shaukat, D. Liu and S. L. Gregory (2015). Sterile inflammation in Drosophila.Mediators of Inflammation 2015, doi:10.1155/2015/369286. Impact 3.2
Z. Shaukat, D. Liu, A. Choo, R. Hussain, L. O'Keefe, R.I. Richards, R.B. Saint, and S.L. Gregory (2014). Chromosomal instability causes sensitivity to metabolic stress.
Oncogene DOI: 10.1038/onc.2014.344 Impact 8.6 Citations: 2
H. Wong, Z. Shaukat, J-B. Wang, R. Saint and S. Gregory (2013). JNK signaling is needed to tolerate chromosomal instability.
Cell Cycle 13:108-117 Impact 5.2 Citations: 4
H. Wong, Z. Shaukat, J Wang, S. Gregory and R. Saint (2013). JNK signaling allows chromosomal instability to be tolerated.
Clinical and Experimental Pharmacology and Physiology 40:S1-15
Z. Shaukat, H. Wong, S. Nicolson, R. Saint and S. Gregory (2012). A screen for selective killing of cells with Chromosomal Instability induced by a spindle checkpoint defect.
PLoS One 7:e47447 Impact 4.1 Citations: 8
Z.I. Bassi, K.J. Verbrugghe, L. Capalbo, S. Gregory, E. Montembault, D.M. Glover and P.P. D’Avino (2011). Sticky/Citron Kinase maintains proper RhoA localization at the cleavage site during cytokinesis.
Journal of Cell Biology 195:595-603. Impact 9.6 Citations: 18
S.L.Gregory and R. Saint (2011)
Cytokinesis. In:Encyclopedia of Life Sciences (ELS). John Wiley and Sons Ltd, Chichester.
S. Ebrahimi and S. L. Gregory (2011). Dissecting protein interactions during cytokinesis.
Communicative and Integrative Biology 4:1-2 Citations:3
S. Ebrahimi, H. Fraval, M. Murray, R. Saint and S. L. Gregory (2010). Polo kinase interacts with RacGAP50C and is
required to localized the cytokinesis initiation complex.
Journal of Biological Chemistry 285:28667-28673. Impact 5.3 Citations: 8
S. L. Gregory, N. Loresuhewa and R. Saint (2010). Signalling through the RhoGEF Pebble in Drosophila.
62:290-295 Impact 2.4 Citations: 7
S. L. Gregory, S. Ebrahimi, J. Milverton, W. H. Jones, A. Bejsovec and R. Saint (2008). Cell division requires a direct interaction between microtubule-associated RacGAP and the contractile ring component Anillin.
Current Biology 18:25-29. Impact 11.0 Citations 96
S. L. Gregory, T. Shandala, L. O’Keefe, L. Jones, M. J. Murray and R. Saint (2007). A Drosophila overexpression screen for modifiers of Rho signaling in cytokinesis.
Fly 1:13-22 Impact 1.2 Citations 21
S. L. Gregory, T. Shandala, H. Dalton and R. Saint (2005). Rho signalling in cytokinesis.
Mechanisms of Development 122:S143. Impact: 3.3
S. L. Gregory, T. Shandala and R. Saint (2005). Regulation of Rho small GTPase signaling during cell division. In “Signal Transduction of Cell Division”, T Miki, ed. Research Signpost Press. pp285-305.
T. Shandala, S. L. Gregory, H. E. Dalton, M. Smallhorn and R. Saint (2004). Citron kinase is an essential effector of the Pbl-activated Rho signalling pathway in Drosophila melanogaster.
Development 131:5053-5063. Impact: 7.6, Citations: 40
N. H. Brown, S. L. Gregory, W. L. Rickoll, L. I. Fessler, M. Prout, R. A. H. White and J. W. Fristrom (2002). Talin is essential for integrin function in Drosophila.
Developmental Cell 3:569-579. Impact: 14.8, Citations: 210
K. Roeper, S. L. Gregory and N. H. Brown (2002). The 'Spectraplakins': cytoskeletal giants with characteristics of both spectrin and plakin families.
Journal of Cell Science 115:4215-4225. Impact: 7.2, Citations: 121
N. H. Brown, S. L. Gregory and M. D. Martin-Bermudo (2000). Integrins as mediators of morphogenesis in Drosophila.
Developmental Biology 223:1-16. Impact: 5.3, Citations: 127
S. L. Gregory (2000). Fly methods for the new millennium.
Nature Cell Biology 2:E211 Impact: 20.2
C. G. Zervas, S. L.Gregory and N. H. Brown (2000). Drosophila Integrin Linked Kinase is required at sites of Integrin adhesion to link the cytoskeleton to the plasma membrane.
Journal of Cell Biology 152:1007-1018. Impact: 12.2 Citations: 262
T. Shandala, R. D. Kortschak, S. L. Gregory and R. Saint (1999). The Drosophila dead ringer gene is required for normal embryonic patterning through regulation of argos and buttonhead.
Development 126:4341-4349. Impact: 7.6 Citations: 37
S. L. Gregory and N. H. Brown (1998). Kakapo, a gene required for adhesion between and within cell layers in Drosophila, encodes a large cytoskeletal linker protein related to Plectin and Dystrophin.
Journal of Cell Biology 143:1271-1282. Impact: 12.2 Citations: 135
S. L. Gregory, R. D. Kortschak, B. K. Kalionis and R. Saint (1996). Characterisation of the dead ringer gene identifies a novel, highly conserved family of sequence specific DNA-binding proteins.
Molecular and Cellular Biology 16:792-799. Impact: 8.1 Citations: 133
J. A. Dibbens, S. L. Gregory and J. B. Egan (1992). Control of gene expression in the temperate coliphage 186. The cI repressor directly represses transcription of the late control gene.
Molecular Microbiology 6:2643-2650. Impact: 5.5 Citations: 13
Genetics Society of Australia
Genetics Society of America
To link to this page, please use the following URL: http://www.adelaide.edu.au/directory/stephen.gregory