As part of the embryo maturation process, orthodox seeds undergo a developmentally regulated dehydration period. The LATE EMBRYOGENESIS ABUNDANT (LEA) genes encode a large and diverse family of proteins expressed during this time. Many hypothesize that LEA proteins act by mitigating water loss and maintaining cellular stability within the desiccated seed, although the mechanisms of their actions remain largely unknown. The model plant Arabidopsis (Arabidopsis thaliana) contains two genes belonging to the group 1 LEA family, ATEM1 and ATEM6, and knockout mutations in these genes are being sought as a means to better understand group 1 LEA protein function during embryo maturation. We have identified a T-DNA insertion allele of the ATEM6 gene in which the T-DNA is present just downstream of the protein coding region. While this gene is transcriptionally active and encodes a wild-type protein, there is no detectable ATEM6 protein in mature seeds. Mutant seeds display premature seed dehydration and maturation at the distal end of siliques, demonstrating that this protein is required for normal seed development. We propose that one function for group 1 LEA proteins in seed development is to buffer the water loss that occurs during embryo maturation and that loss of ATEM6 expression results in the mutant phenotype.

The end of orthodox seed development is typified by a developmentally regulated period of dehydration leading to the loss of bulk water from the entire structure. When dehydration occurs, the cytoplasm condenses and intracellular components become more crowded, providing an environment amenable to numerous undesirable interactions that can lead to protein aggregation, denaturation and organelle-cell membrane fusion. Acquisition of desiccation tolerance, or the ability to withstand these very low water potentials and consequent molecular crowding, has been correlated with the accumulation of various protective compounds including proteins and sugars. Among these are the late embryogenesis abundant (LEA) proteins, a diverse class of highly abundant, heat-stable proteins that accumulate late in embryo maturation coincident with the acquisition of desiccation tolerance. Previous work led us to hypothesize that the protein ATEM6, one of the two Arabidopsis thaliana group 1 LEA proteins, is involved in regulating the rate at which water is lost from the maturing embryo; homozygous atem6-1 mutants display premature dehydration of seeds at the distal end of the silique. Here we demonstrate that rehydrated, mature seeds from atem6-1 mutant plants lose more water during subsequent air drying than wild-type seeds, consistent with a role for ATEM6 protein in water binding/loss during embryo maturation. In addition, and possibly as a result of premature dehydration, mutant seeds along the entire length of the silique acquire desiccation tolerance earlier than their wild-type counterparts. We further demonstrate precocious, and perhaps elevated, expression of the other A. thaliana group 1 LEA protein, ATEM1, that may compensate for loss or ATEM6 expression. However, this observation could also be consistent with acceleration of the entire normal maturation program in atem6-1 mutant embryos. Interestingly, ATEM6 protein does not appear to be required in mature seeds for viability or efficient germination.

Evidence going as far back as the early part of the 20th century suggests that both light and chloroplast function may play key roles in host susceptibility to viruses. Despite the long history of such work, confirmation of these phenomena and a determination of the underlying mechanisms remain elusive. Here, we revisited these questions using modern imaging technologies to study the susceptibility of Nicotiana benthamiana to Turnip mosaic virus (TuMV). We found that both light deficiency and photosystem impairment increased the susceptibility of N. benthamiana to TuMV infection. Time-lapse photography studies indicated that, under these conditions, rub-inoculated plants exhibited greater numbers of infection foci and more rapid foci development. The rate of systemic movement was also accelerated though cell-to-cell movement appeared unchanged. Inhibition of salicylic acid (SA)-mediated defense responses is not likely responsible for changes in susceptibility because SA and pathogen response-1 gene induction were not affected by light deficiency or chloroplast impairment and treatment of plants with SA had no measureable impact on TuMV infection. Taken together, these data suggest that both light and optimal chloroplast function influence virus infection either by limiting the cellular resources needed by TuMV to establish replication complexes or the host's ability to activate SA-independent defenses.

No abstract