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Jeanne M. Harris Research Program


Role of the LATD gene in root meristem function and ABA signaling.

Nodule and lateral root development is defective in latd mutants. Arrowheads indicate nodules; arrows lateral roots.

We have identified a gene in Medicago truncatula, LATD, that is required for the growth of both primary and lateral root meristems as well as that of symbiotic root nodules. In mutants lacking LATD function, the primary root initially appears wild-type, but the root tip becomes increasingly abnormal and by 22 days growth ceases. Arrested root tips have abnormal meristems and highly disorganized root caps. Lateral root growth is more severely affected: most lateral roots never exhibit a period of growth, but rather arrest soon after emergence from the parent root. DAPI staining reveals extensive disorganization of arrested lateral roots. Similarly, nodules arrest near the time of emergence from the primary root and appear to lack a meristematic region.

Surprisingly, we have found that 1-10 µM ABA rescues the growth defects and meristematic disorganization of both primary and lateral roots, but not arrested nodules. We found that latd mutants make normal levels of ABA, so these defects in root growth are not due to a lack of ABA. If the root defects in latd mutants are due to a reduced ability to sense ABA, then the plants should exhibit other ABA-insensitive phenotypes. In fact, we found that latd mutants have two classic ABA-insensitive phenotypes: failure to close stomata in response to ABA and reduced inhibition of seed germination by ABA. We are currently examining the effect of the latd mutation on ABA-regulated gene expression.

The latd root phenotype is rescued by 1 µM ABA.

Our finding that LATD links lateral root development, nodule formation and ABA signaling in legumes raises several questions. No gene with a similar function has been described in any plant to date. What is the sequence of the LATD gene? Are there homologs in non-legumes? What is the molecular function of the LATD gene product? Where is it localized in the plant or the cell? To answer these questions, our lab is cloning the LATD gene using a map-based approach in collaboration with Rebecca Dickstein's lab at the University of North Texas. We have currently mapped the LATD gene to the top of Linkage Group 1 and have identified closely linked molecular markers.

Finally, what is the relationship of the LATD gene to the evolution of nodulation? Since the altered ABA responsiveness of lateral roots appears to be linked to the evolution of nodulation phylogenetic analysis of the LATD gene will prove to be very illuminating.

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