Joel L. Sachs

Associate Professor and Vice Chair of Biology
Office: Boyce Hall, Room 5406
Office phone: (951) 827-6357
Lab phone: (951) 827-3455
Facsimile: (951) 827-4286


Lab Website

2012-2017   NSF CAREER Award(DEB/IOS)
2008-2011   NSF Award ~ Division of Environmental Biology
2006-2007   NIH Ruth Kirschstein National Research Service Award
2004            Bess Heflin Fellow
2003             Carl Gottfried Hartman Fellow
2003            NSF Doctoral Dissertation Improvement Grant

Degree:   Ph.D., University of Texas at Austin, 2004

Research Interests

  • Evolutionary-Ecological genomics of beneficial bacteria
  • Coevolution of rhizobial-legume symbioses
  • Origins of harmful strains in symbiont populations
  • Macroevolution of symbiotic cooperation

    Symbiotic bacteria are a key yet poorly understood facet of our natural world. Yet humans and our food sources often depend on bacterial cooperation for health and fitness. Current research is beginning to unravel the molecular and selective basis of bacterial cooperation. In the process we are discovering that beneficial infections are often evolutionarily unstable and more dynamic than expected. In the Sachs Lab we investigate the forces that shape bacterial cooperation with hosts as well as the origins and evolution of harmful strains. Our current focus is on rhizobial bacteria that live in soils throughout the world and nodulate the roots of many legume hosts. Projects in the Sachs Lab often utilize a wide range of techniques to answer basic questions. These include field collections of wild bacteria, experimental infections and experimental evolution, whole genome sequencing and phylogenetic analysis. Below are several broad research themes that we are currently investigating:

    Evolutionary genomics and the origins of symbiosis
    The advent of next-gen and whole-genome sequencing is allowing unforeseen advances in evolutionary biology. For the study of symbioses in particular, these approaches are allowing biologists to begin to resolve the genetic mechanisms that drive the origins, maintenance and breakdown of symbiotic interactions. We use genomic data to test evolutionary genetic hypotheses about the different trajectories of bacterial mutualists and pathogens, to reconstruct extremely well resolved phylogenies and to examine the genomic changes that occur in during evolutionary transitions in host association.

    The origins of uncooperative symbionts
    Rhizobia are bacteria that fix nitrogen in legume roots in exchange for photosynthates from their hosts. However, non-beneficial rhizobia are widespread, including non-fixing strains that appear to be cheaters and non-nodulating strains that fail to infect hosts. Recent research has shown that legumes can punish some uncooperative rhizobia and substantially reduce their fitness, but these sanctions must not be universally effective. Important questions about uncooperative rhizobia remain unresolved. (i) Is it adaptive for rhizobia to be uncooperative with hosts? (ii) Do uncooperative rhizobia evolve from cooperative ancestors? (iii) What are the mechanisms of rhizobial exploitation? We are using experimental approaches as well as phylogenetic analyses to address these key gaps in our knowledge.

    Host control over uncooperative symbionts
    Host control mechanisms are thought to be critical for selecting against cheater mutants in symbiont populations. Some of our recent research has tested a legume host's ability to constrain the infection and proliferation of a native occurring rhizobial cheater (see below). Lotus strigosus hosts were experimentally inoculated with pairs of Bradyrhizobium strains that naturally vary in symbiotic benefit, including a cheater symbiont strain that proliferates in the roots of singly-infected hosts yet provides zero growth benefits. Within coinfected hosts, the cheater exhibited lower infection rates than competing beneficial strains and grew to smaller population sizes within those nodules. In vitro assays revealed that infection-rate differences among competing strains were not due to variation in rhizobial growth rate or inter-strain toxicity. These results can explain how a rapidly growing cheater symbiont -- that exhibits a massive fitness advantage in single infections -- can be prevented from sweeping through a beneficial population of symbionts. We are now testing how these control mechanisms evolve and how they are perturbed by ecological changes such as anthropogenic nitrogen deposition.

    Dr. Sachs participates in the Ecology and Evolutionary Biology tracks of the Evolution, Ecology and Organismal Biology graduate program (EEOB), as well as the graduate programs in Microbiology (Micro), Genetics, Genomics & Bioinformatics (GGB) and Cell, Molecular, and Developmental Biology.

    Selected Recent Publications: (PDFs available at Sachs Lab Website)

    Postdoctoral Research opportunities

    Graduate Research opportunities

    Undergraduate Research Opportunities

    CV [PDF file]