This work sheds lights on the complex gene regulatory networks underlying heat stress response and tolerance in chickpea ( Cicer arietinum L.) using a transcriptomic approach integrated with key phenotypic traits. Two pairs of Near Isogenic Lines (NILs) derived from a cross between early- (E) and late-flowering (L) genotypes (224E, 224L, 309E and 309L) and a reference cultivar ICC 4958 were subjected to high temperature (38/28 oC (day/night) for 4 days during the pod set) during the seed-filling stage, Heat stress impacted seed yield, revealing significant differences between early and late flowering lines primarily by reducing seed number due to fertilization failure. The ICC 4958 and 224L genotypes were more severely affected than the 309E and L and 224E lines. The differential gene expression profiles highlighted genotype-specific responses to heat stress, with both the 309 lines exhibiting greater heat tolerance and fewer differentially expressed genes compared to 224E, 224L and ICC 4958, indicating their higher resilience to heat stress. Key responses included significant changes in photosynthesis-related genes, alterations in primary and secondary metabolism, and modulation of phytohormone pathways, which collectively contribute to the 309 lines’ ability to cope with and recover from heat stress. The efficient recovery mechanisms observed in early flowering lines, such as rapid re-establishment of photosynthetic functions and effective nutrient redistribution, underline their potential for maintaining yield under heat stress conditions.

In this work, we describe the results obtained in the model plant, Arabidopsis thaliana, to investigate the transgenerational phenotypic effects of chromium (Cr) stress. F1 generation from parents grown in both acute and chronic stress showed significant higher levels of the maximal effective concentration (EC50) than F1 from unstressed parents. In addition, both F1 from Cr stressed parents showed higher germination rate under Cr presence and F1 from parents cultivated under chronic stress displayed reduction of hydroxide peroxide levels under Cr stress compared to control. At lower Cr stress level, F1 resulted to promptly activate more genes involved in Cr stress responses than F0 implying a memory linked to a transgenerational priming. F1 modulated significantly less genes than F0 at later stage and at higher Cr levels implying a memory leading to Cr stress adaptation. Several members of bHlH transcription factors were induced by Cr stress in F1 and not in F0, such as bHlH100, ORG2 and ORG3. F1 optimized gene expression towards pathways linked to iron starvation response. A model of transcriptional regulation of transgenerational memory to Cr stress was developed and eventually applied for other heavy metal stresses.