Auxin homeostasis is maintained by sly-miR167-SlARF8A/B-SlGH3.4 feedback module in the development of locular and placental tissues of tomato fruits.

The locular gel, produced by the placenta, is important for fruit flavor and seed development in tomato. However, the mechanism underlying locule and placenta development is not fully understood yet. Here, we show that two SlARF transcription factors, SlARF8B and SlARF8A (SlARF8A/B), promote the development of locular and placenta tissues. The expression of both SlARF8A and SlARF8B is repressed by sly-microRNA167 (sly-miR167), allowing for the activation of auxin downstream genes. In slarf8a, slarf8b, and slarf8a/b mutants, the auxin (IAA) levels are decreased, whereas the levels of inactive IAA conjugates including IAA-Ala, IAA-Asp, and IAA-Glu are increased. We further find that SlARF8B directly inhibits the expression of SlGH3.4, an acyl acid amino synthetase that conjugates the amino acids to IAA. Disruption of such auxin balance by the increased expression of SlGH3.4 or SlGH3.2 results in defective locular and placental tissues. Taken together, our findings reveal an important regulatory module constituted by sly-miR167-SlARF8A/B-SlGH3.4 during the development of locular and placenta tissues of tomato fruits.

Time-course observation of the reconstruction of stem cell niche in the intact root.

The stem cell niche (SCN) is critical in maintaining continuous postembryonic growth of the plant root. During their growth in soil, plant roots are often challenged by various biotic or abiotic stresses, resulting in damage to the SCN. This can be repaired by the reconstruction of a functional SCN. Previous studies examining the SCN's reconstruction often introduce physical damage including laser ablation or surgical excision. In this study, we performed a time-course observation of the SCN reconstruction in pWOX5:icals3m roots, an inducible system that causes non-invasive SCN differentiation upon induction of estradiol on Arabidopsis (Arabidopsis thaliana) root. We found a stage-dependent reconstruction of SCN in pWOX5:icals3m roots, with division-driven anatomic reorganization in the early stage of the SCN recovery, and cell fate specification of new SCN in later stages. During the recovery of the SCN, the local accumulation of auxin was coincident with the cell division pattern, exhibiting a spatial shift in the root tip. In the early stage, division mostly occurred in the neighboring stele to the SCN position, while division in endodermal layers seemed to contribute more in the later stages, when the SCN was specified. The precise re-positioning of SCN seemed to be determined by mutual antagonism between auxin and cytokinin, a conserved mechanism that also regulates damage-induced root regeneration. Our results thus provide time-course information about the reconstruction of SCN in intact Arabidopsis roots, which highlights the stage-dependent re-patterning in response to differentiated quiescent center.

H and HL synergistically regulate jasmonate-triggered trichome formation in tomato.

The development of trichomes, which protect plants against herbivores, is affected by various stresses. In tomato, previous studies showed that stress triggered JA signaling influences trichome formation, but the underlying mechanism is not fully resolved. Here, we found two C2H2 zinc finger proteins synergistically regulate JA-induced trichome formation in tomato. The naturally occurring mutations in H and its close homolog H-like gene in a spontaneous mutant, LA3172 cause severely affected trcihome development. Compared with respective single mutant, h/hl double mutant displayed more severe trichome defects in all tissues. Despite the partially redundant function, H and HL genes regulate the trichome formation in the spatially distinct manner, with HL more involved in hypocotyls and leaves, while H more involved in stems and sepals. Furthermore，the activity of H/HL is essential for JA-triggered trichome formation. JA signaling inhibitor SlJAZ2 represses the activity of H and HL via physical interaction, resulting in the activation of THM1, a negative regulator of trichome formation. Our results provide novel insight into the mechanism of the trichome formation in response to stress induced JA signaling in tomato.