Robert M. Larkin
Assistant Professor
  • Ph.D. 1996, University of Missouri
larkinr@msu.edu
S206 Plant Biology Building
Michigan State University
East Lansing, MI 48824
Office: 517-432-4619
Lab: 517-432-4621
Fax: (517) 353-9168


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Robert M. Larkin

Research Interests

Molecular and Genetic Analysis of Plastid-to-Nucleus Signaling Pathways

We study signal transduction and gene regulation in plants focusing on signals from plastids such as the chloroplast that regulate the expression of nuclear genes that encode proteins active in photosynthesis.

Plastids are small organelles that perform photosynthesis and a number of other essential functions in plant cells. Although plastids contain genomes that encode a small percentage of plastid-localized proteins, the overwhelming majority of plastid-localized proteins are encoded by nuclear genes. Therefore, regulation of nuclear gene expression in response to developmental and environmental cues plays an important role in plastid development and function. Extraplastidic signaling pathways that regulate nuclear gene expression do not have absolute control over plastid development and function. Plastids send signals to the nucleus that are essential for the proper expression of nuclear genes.   For example, particular chloroplast signals fine tune the expression of nuclear genes that encode components of the photosynthetic machinery to particular light environments; other chloroplast signals induce cytoplasmic antioxidant defense proteins as reactive oxygen species accumulate within the chloroplast.  Plastid signals couple the expression of nuclear genes that encode proteins active in photosynthesis to the functional state of the chloroplast and help coordinate the expression of the nuclear and chloroplast genomes.  Plastid signals are some of the most important and poorly understood signals that regulate photosynthesis-associated nuclear genes (PhANGs).  A more thorough understanding of the interactions between plastid signals and extraplastidic signaling pathways will contribute to our understanding of signal transduction networks and the regulation of photosynthesis.

We have two projects in our laboratory.  The first project aims to understand the regulation of photosynthesis-associated genes by plastid signals.  The regulation of these genes is complex, involving pathways triggered by light, the circadian clock, tissue-specific signals, carbohydrates, hormones, and plastids. The mechanisms plants use to integrate all of these signals are poorly understood.  Our recent findings indicate that plastid signals control the activity of particular light signaling pathways that regulate PhANGs and can change the response PhANGs to light quality and quantity. Plastid signals rewire light signaling pathways at least in part by converting HY5, which is a transcription factor that acts downstream of photoreceptors in light signaling pathways, from a positive to a negative regulator of PhANGs (Figure 1).

Figure 1. The rewiring of a blue light signaling pathway by plastid signals. (A) The regulation of PhANGs by blue light when chloroplast biogenesis and photosynthesis are optimal. Blue light is perceived by the photoreceptor cryptochrome 1 (cry1) which in turn inhibits COP1, which is an E3 ubiquitin ligase that targets HY5 for degradation by the proteasome. HY5 is basic-leucine zipper type transcription factor and a positive regulator of particular PhANGs when chloroplast biogenesis and photosynthesis are optimal. (B) The regulation of PhANGs by blue light when chloroplasts are damaged. When chloroplast biogenesis and photosynthesis are suboptimal, HY5 can negatively regulate the same PhANGs that it positively regulates when chlororoplast biogenesis and photosynthesis are optimal. In our current working model, a signal (X) from the damaged chloroplast converts HY5 into a repressor of PhANGs by a mechanism that remains an open question but may involve posttranslational modifications, heterodimerization with distinct transcription factors, changes in the concentrations of coactivators and corepressors, or some combination of these mechanisms. A distinct plastid-to-nucleus signaling pathway that contains the GUN1 protein also represses PhANG expression under these conditions.

These findings indicate that a signaling network made up of plastid and light signaling pathways allows plants to integrate signals that describe particular light environments and signals that describe the functional and developmental state of the chloroplast when regulating PhANG expression. Integrating these environmental and endogenous signals is expected to help plants more effectively regulate chloroplast biogenesis and photosynthesis.   MORE

Recent Publications

Ruckle ME, Demarco SM, Larkin RM (2007) Plastid signals remodel light signaling networks and are essential for efficient chloroplast biogenesis in Arabidopsis. Plant Cell 19: 3944-3960. Link to pdf

Verdecia MA, Larkin RM, Ferrer JL, Riek R, Chory J, Noel JP (2005) Structure of the Mg-Chelatase Cofactor GUN4 Reveals a Novel Hand-Shaped Fold for Porphyrin Binding. PLoS Biol. 3(5):e151 DOI: 10.1371/journal.pbio.0030151. Link to pdf

Larkin, R.M., Alonso, J.M., Ecker, J.R. and Chory, J. (2003) GUN4, a regulator of chlorophyll synthesis and intracellular signaling. Science 299, 902-906. Link to pdf

Mochizuki N., Brusslan J.A., Larkin R., Nagatani, A. and Chory, J. (2001) Arabidopsis genomes uncoupled 5 (GUN5) mutant reveals the involvement of Mg-chelatase H subunit in plastid-to-nucleus signal transduction. Proc. Natl. Acad. Sci. USA 98, 2053-2058. Link to pdf