SummaryChanges in the degree of fatty acid (FA) desaturation are implicated in plant responses to various abiotic stresses, including heat, salt and drought. However, it is still not known whether decreased levels of linolenic acid, found in many plants subjected to salt and drought stress, reflect a mechanism of defence or damage. We addressed this question by generating tobacco cells and plants ectopically overexpressing two FA desaturases: the cytosolic FAD3 or the plastidic FAD8. A remarkable increase in the ratio of total linolenic to linoleic acids resulted from overexpression of FAD3, whereas ectopic overexpression of FAD8 induced an increased ratio mainly in the plastidic lipids. Here we present evidence that overexpressing FAD8 imposes much greater heat sensitivity than does FAD3 overexpression, in both cultured cells and whole plants. Overexpression of either FAD3 or FAD8 increases tolerance to drought in tobacco plants and to osmotic stress in cultured cells. These findings suggest that a drought-induced decreased level of linolenic acid reflects damage. Our results point to the potential of exploiting FAD overexpression as a tool to ameliorate drought tolerance.

SummaryThe extreme sensitivity of the microsporogenesis process to moderately high or low temperatures is a major hindrance for tomato (Solanum lycopersicum) sexual reproduction and hence year‐round cropping. Consequently, breeding for parthenocarpy, namely, fertilization‐independent fruit set, is considered a valuable goal especially for maintaining sustainable agriculture in the face of global warming. A mutant capable of setting high‐quality seedless (parthenocarpic) fruit was found following a screen of EMS‐mutagenized tomato population for yielding under heat stress. Next‐generation sequencing followed by marker‐assisted mapping and CRISPR/Cas9 gene knockout confirmed that a mutation in SlAGAMOUS‐LIKE 6 (SlAGL6) was responsible for the parthenocarpic phenotype. The mutant is capable of fruit production under heat stress conditions that severely hamper fertilization‐dependent fruit set. Different from other tomato recessive monogenic mutants for parthenocarpy, Slagl6 mutations impose no homeotic changes, the seedless fruits are of normal weight and shape, pollen viability is unaffected, and sexual reproduction capacity is maintained, thus making Slagl6 an attractive gene for facultative parthenocarpy. The characteristics of the analysed mutant combined with the gene's mode of expression imply SlAGL6 as a key regulator of the transition between the state of ‘ovary arrest’ imposed towards anthesis and the fertilization‐triggered fruit set.

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The molecular signals for the development of the ovary into fruit following ovule fertilization are not clear. However, in many species, including tomato ( Lycopersicon esculentum Mill.), auxins and auxin transport inhibitors can substitute for fertilization as activators of fruit set, suggesting that this plant hormone plays a key role in this process. In agreement, transgenes for auxin biosynthesis expressed under ovary- or ovule-specific promoters were shown earlier to enable parthenocarpic (i.e. seedless) fruit development. In the present study, we tested an alternative approach for the induction of parthenocarpy that is based on ovary-specific expression of the Agrobacterium rhizogenes-derived gene rolB. This gene was chosen because rolB transgenic plants manifest several syndromes characteristic of auxin treatment. Tomato plants transformed with a chimeric construct containing the rolB gene fused to the ovary- and young-fruit-specific promoter TPRP-F1 developed parthenocarpic fruits. Fruit size and morphology, including jelly fill in the locules of the seedless fruits, were comparable to those of seeded fruits of the parental line. Although it is not known whether ROLB signals for the same cassette of genes involved in fertilization-dependent fruit development, it clearly activates a battery of genes that enable successful completion of seedless fruit development in tomato.

). † These authors contributed equally to this work. SUMMARYWe previously identified SlFSM1 as an early fruit-specific gene encoding a short protein harboring a noncanonical SANT/MYB-like domain. Here, we investigated the role of FSM1 during fruit development in tomato and its mode of action. By analyzing tomato plants ectopically expressing FSM1, we established that it negatively affects cell expansion, particularly of those cells with the highest potential to expand, such as those residing inner to the vascular bundles in the fruit pericarp. This function of FSM1 differs from that of the snapdragon FSM1-like gene, RAD, which through an antagonistic activity with DIV participates in establishing floral asymmetry. Revealing an additional component of the FSM1/RAD regulatory complex, we show here that FSM1 physically interacts with FSB1, a previously uncharacterized factor harboring an atypical MYB repeat. We also demonstrate that FSB1 physically interacts with the transcription factor MYBI, a homolog of DIV. Our results show that the formation of the FSB1-MYBI complex is competed by FSM1, which recognizes in FSB1 the same region as MYBI does. Taken together, these studies expose a function for the FSM1/FSB1/ MYBI complex in controlling tomato cell expansion, while revealing a mechanism by which competing MYB-MYB interactions could participate in the control of gene expression.