Roger Jacobs, Ph.D.
- Ghaemi R, Arefi P, Stosic A, Acker M, Raza Q, Jacobs JR and Selvaganapathy PR. (2017) A microfluidic microinjector for toxicological and developmental studies in Drosophila embryos. Lab Chip, 2017, http://dx.doi.org/10.1039/C7LC00537G
- Hughes, CJR and Jacobs, JR (2017) Dissecting the Role of the Extracellular Matrix in Heart Disease: Lessons from the Drosophila Genetic Model. Vet. Sci. 2017, 4, 24; doi:10.3390/vetsci4020024
- Vanderploeg J, Jacobs JR (2017) Mapping heart development in flies: Src42A acts non-autonomously to promote heart tube formation in Drosophila. Vet. Sci. 2017, 4, 23; doi:10.3390/vetsci4020023
- Raza Q, Vanderploeg, J Jacobs JR. (2017) Matrix Metalloproteinases are required for membrane motility and lumenogenesis during Drosophila heart development. PlosONE PLoS Feb 13;12(2):e0171905. http://dx.doi.org/10.1371/journal.pone.0171905
- Raza Q, Jacobs JR (2016) Guidance signalling regulates leading edge behaviour during collective cell migration of cardiac cells in Drosophila. Dev Biol. 419(2):285-297 http://dx.doi.org/10.1016/j.ydbio.2016.09.005
- Bogatan S, Cevik D, Demidov V, Vanderploeg J, Panchbhaya A, Vitkin A, Jacobs JR.(2015) Talin Is Required Continuously for Cardiomyocyte Remodeling during Heart Growth in Drosophila. PLoS One. 2015 Jun 25;10(6)
- Vanderploeg J, Jacobs JR.(2015) Talin is required to position and expand the luminal domain of the Drosophila heart tube. Dev Biol. 2015 Sep 15;405(2):189-201.
- Vanderploeg J, Vazquez Paz LL, MacMullin A, Jacobs JR. (2012) Integrins are required for cardioblast polarisation in Drosophila. BMC Dev Biol. 12:8.
- Knox J, Moyer K, Yacoub N, Soldaat C, Komosa M, Vassilieva K, Wilk R, Hu J,Vazquez Paz Lde L, Syed Q, Krause HM, Georgescu M, Jacobs JR. (2011) Syndecan contributes to heart cell specification and lumen formation during Drosophila cardiogenesis. Dev Biol. 356:279-90.
- Moyer KE, Jacobs, JR. (2008) Varicose: a MAGUK required for the maturation and function of Drosophila septate junctions. BMC Dev Biol. 8:99
- MacMullin A and Jacobs, JR. (2006) Slit coordinates cardiac morphogenesis in Drosophila. Dev Biol. 293:154-64.
- Settle, M., Gordon, M.D., Nadella, M., Dankort, D., Muller, W., Jacobs, J.R. (2003) Genetic identification of effectors downstream of Neu (ErbB-2) autophosphorylation sites in a Drosophila model.Oncogene 22:1916-1926.
- Stevens, A. and Jacobs, J.R. (2002) Integrins Regulate Responsiveness to Slit Repellent Signals J. Neurosci. 22: 4448-4455.
- Battye, R.A., Stevens, A., Perry, R., and Jacobs, J.R. (2001) Repellent signaling from Slit requires the Leucine Rich Region. J. Neurosci . 21:4290-4298
- Jacobs, J.R. (2000) The Midline Glia of Drosophila: A molecular genetic model for the developmental functions of glia. Prog. Neurobiol. 62:475-508
Genetics of cell signaling and development
Our studies are aimed at uncovering the molecules and mechanisms that regulate cell differentiation, and morphogenesis during development. We address these issues in Drosophila, a model organism with state- of-the-art tools to assess gene function and manipulate gene expression in vivo. Our focus is the morphogenesis, growth and aging of the Drosophila heart. The genetic and molecular mechanisms are highly conserved between Drosophila and mammals. Insights into mechanism are relevant to studies of congenital cardiomyopthies and disorders of cardiac aging, such as cardiac hypertrophy.
Guidance Signaling during heart morphogenesis
We previously demonstrated how Slit, a glycoprotein secreted by the nervous system midline, acts as a repellent signal to guide the extension of developing axons in the CNS. Our current studies reveal that Slit also works to guide cell movement and shape change essential to forming the Drosophila heart. Without Slit, heart cells cannot align themselves properly to build the heart tube. Furthermore, Slit is required for the heart to form an inner chamber (lumen) to carry the blood. Significantly, Slit function in the heart is closely linked to adhesion signals and the extracellular matrix. We are using molecular and genetic techniques to explore how adhesion signals affect the cell shape changes as the heart is formed. The composition of the extracellular matrix changes with growth and aging. We are examining what signals and physiological circumstances regulate these changes.
Left: sparse fibrils of ECM protein Pericardin (green) overlie the contractile cardiomyocytes (actin-red)
Right: Altered cardiomyocyte adhesion and contraction results in heavier deposition of Pericardin