Dr Gregory Jedd, Principal Investigator

Gregory Jedd was educated at Foothill Community College in California and later earned his bachelors degree in biology at Stanford University. He received his PhD from the University of Chicago and did his postdoctoral work in Nam-Hai Chua’s lab at the Rockefeller University where he developed an interest in the cell and evolutionary biology of filamentous fungi.  In September of 2004 he moved to Singapore to establish the Comparative Cell Biology Group.

You may wish to contact Dr Gregory JEDD at:
Tel: (65) 6872 7000, 6872 7708 or 6872 7709(DID) Email: gregory@tll.org.sg

For information on PhD studies at TLL, click HERE

• Peroxisome and Woronin body formation and function
• Cell polarity and development of filamentous fungi
• Fungal evolution
• Novel matrix-forming structural proteins

Research Projects

My laboratory uses filamentous fungi as model organisms for the investigation of basic biological questions relating to organelle assembly, cell polarity, multicellular development and the evolution of fungal life styles.  Also, by focusing on unique aspects of the fungal cell, our work is aimed at developing new strategies for combating fungal pathogens.
Adaptation is frequently associated with the advent of new cellular and organellar function and in many cases these innovations can be mapped to nodes on phylogenetic trees, suggesting that they arose in a common ancestor upon whom they conferred a significant advantage. In one aspect of our work, we employ a multidisciplinary approach to investigate these functions.
We are particularly interested in multicellular coenocytic filamentous fungi. In these systems, individual cells are connected by perforate septa, which allow intercellular cooperation and communication and major groups of filamentous fungi have evolved distinct septal pore-associated organelles. In one approach, these organelles are biochemically purified and cellular and genetic techniques are subsequently used to determine the function of constituent proteins. In a complementary approach, genetic screens are employed to identify genes controlling organelle assembly and function. Currently, we are studying the biogenesis and function of a peroxisome derived organelle known as the Woronin body (see below).  In addition, we are investigating the genetic and cellular mechanisms that control fungal cell polarity using Neurospora crassa as a model system.

The Fungal Colony

Filamentous fungi grow through polarized tip extension, resulting in tubular cells (hyphae) that further branch and fuse, resulting in a network of interconnect hyphae (Fig. 1).  In most filamentous fungi, cells are formed by the regular formation of perforate septa, which allow intercellular communication.  This syncytial lifestyle allows cellular cooperation and is probably important for rapid invasive growth and the elaboration of multicellular reproductive structures. Major groups of filamentous fungi have evolved distinct septal pore-associated organelles.

Figure 1. A typical fungal colony derived from the germination of a single spore. This figure is reproduced from A.H.R. Buller’s, Researches on Fungi.

The Woronin Body

The Euascomycetes are a monophyletic and ecologically diverse group of filamentous fungi that include important plant (e.g. Magnaporthe grisea) and human (e.g. Aspergillus fumigatus) pathogens.  These fungi evolved a septal pore associated organelle known as the Woronin body (named for its discoverer, M. Woronin) and in previous work this organelle was purified from Neurospora crassa.  This allowed us to show that the Woronin body is peroxisome-derived and centered on a novel self-assembled structural protein, HEX-1.  Woronin bodies are absent in a hex-1 deletion mutant and these strains are unable to seal the septal pore in response to cellular damage, revealing an essential function that supports the syncytial lifestyle characteristic of this group.
In collaboration with K. Swaminathan (IMCB, Singapore) and colleagues, the HEX-1 crystal structure has been solved at a resolution of 1.8 Å (Fig. 2) and using this information, we designed assembly-defective mutants.  These mutants allowed us to show that HEX-1 crystallinity is required for Woronin body function.  Current efforts are focused on understanding how Woronin bodies are formed from the peroxisome and the mechanism of Woronin body-assisted membrane resealing.  Towards this end, we are exploiting the excellent molecular and classical genetics of Neurospora to isolate and characterize mutants defective in Woronin body formation and function.

 
Figure 2. The Woronin body of Neurospora crassa (upper left and lower right, by light microscopy.  Diameter = approximately 1mm) and an assembly of 84 HEX-1 monomers derived from the crystal structure.  This model is being used to design mutations that alter physical properties of the Woronin body-core.

Genetic differentiation of the fungal hypha

We have recently shown that polarized gene expression determines Woronin body formation in apical hyphal compartments (Fig. 3, Tey et. al., 2005) and we further defined a sub-apical pattern of gene expression (also observed by Moukha et. al. (1993) J. Bacteriology, 175, 3672-3687).  Together, these data show that hyphae are genetically differentiated along their length.  Our goal is to eventually understand how this differentiation is established and maintained to control and coordinate regional cellular activity within the fungal colony.

Figure 3.  hex-1 gene expression is polarized. High levels of expression are indicated by warm colors in this histogram showing the pattern of fluorescence generated when YFP (Yellow Fluorescent Protein) is expressed from hex-1 regulatory sequences.  A singly hypha with several branches is shown.  Scale bar = 0.5 mm.