Qin-Xin Bao

Phosphate (Pi) is an essential nutrient that frequently limits plant growth because of its low availability in soils, especially during early seedling development in Arabidopsis . Under Pi-deficient conditions, etiolated seedlings exhibit elongated hypocotyls, shortened roots, and small, pale cotyledons—a morphological adaptation that enhances light-foraging capacity. However, how Pi is strategically distributed among these organs to optimize seedling establishment remains unclear. We here identify a PHR1-EIN3/EIL1 regulatory module that directs minimal Pi resources to suppress root elongation and cotyledon expansion or to accelerate greening, promoting Pi conservation. This mechanism prioritizes hypocotyl elongation to improve light acquisition. In contrast, under sufficient Pi supply, hypocotyl and root growth is promoted along with cotyledon enlargement, while greening is delayed. Thus, the PHR1-EIN3/EIL1 module enables efficient allocation of limited Pi to maximize hypocotyl elongation for light foraging during early seedling establishment while strategically restricting Pi usage in other organs to enhance overall survival.

Trichome initiation and development is regulated by a diverse range of environmental signals. However, how leaf carbohydrate status determines the trichome initiation and development of systemic developing leaves remains unclear. Here, we found that a specific organ (such as a mature leaf) could function as a nutrient sensor, subsequently promoting or suppressing nonautonomous regulation of trichome initiation and development in response to alternations in nutrient levels. This physical phenomenon was regulated by a sucrose ⟶ ACS7 ⟶ ethylene ⟶ EIN3 ⟶ SUC4 ⟶ sucrose pathway in mature leaves, with a remote control of trichome production in newly developing leaves via a sucrose ⟶ ACS7 ⟶ ethylene ⟶ EIN3 ⟶ TTG1 pathway. These data provide insights into how mature leaves function as nutrient sensors that control trichome formation within distant developing leaves through a nutrient sensor–relay mechanism. Our findings uncover both a previously unidentified, nutrient sensing–regulatory mechanism and the cognate underpinning molecular architecture.

Soil (or plant) water deficit accelerates plant reproduction. However, the underpinning molecular mechanisms remain unknown. By modulating cell division/number, ABSCISIC ACID-INSENSITIVE 5 (ABI5), a key bZIP (basic (region) leucine zippers) transcription factor, regulates both seed development and abiotic stress responses. The KRP (KIP-RELATED PROTEIN) cyclin-dependent kinases (CDKs) play an essential role in controlling cell division, and SHOOT MERISTEMLESS (STM) plays a key role in the specification of flower meristem identity. Here, our findings show that abscisic acid (ABA) signaling and/or metabolism in adjust reproductive outputs (such as rosette leaf number and open flower number) under water-deficient conditions in Arabidopsis (Arabidopsis thaliana) plants. Reproductive outputs increased under water-sufficient conditions but decreased under water-deficient conditions in the ABA signaling/metabolism mutants abscisic acid2-1 (aba2-1), aba2-11, abscisic acid insensitive3-1 (abi3-1), abi4-1, abi5-7, and abi5-8. Further, under water-deficient conditions, ABA induced-ABI5 directly bound to the promoter of KRP1, which encodes a CDK that plays an essential role in controlling cell division, and this binding subsequently activated KRP1 expression. In turn, KRP1 physically interacted with SHOOT MERISTEMLESS (STM), which functions in the specification of flower meristem identity, promoting STM degradation. We further demonstrate that reproductive outputs are adjusted by the ABI5-KRP1-STM molecular module under water-deficient conditions. Together, our findings reveal the molecular mechanism by which ABA signaling and/or metabolism regulate reproductive development under water-deficient conditions. These findings provide insights that may help guide crop yield improvement under water deficiency.

Exposure of dark-grown etiolated seedlings to light triggers the transition from skotomorphogenesis/etiolation to photomorphogenesis/de-etiolation. In the life cycle of plants, de-etiolation is essential for seedling development and plant survival. The mobilization of soluble sugars (glucose, sucrose and fructose) derived from stored carbohydrates and lipids to target organs, including cotyledons, hypocotyls and radicles, underpins de-etiolation. Therefore, dynamic carbohydrate biochemistry is a key feature of this phase transition. However, the molecular mechanisms coordinating carbohydrate status with the cellular machinery orchestrating de-etiolation remain largely opaque. Here, we show that the glucose (Glc) sensor HEXOKINASE1 (HXK1) interacts with GROWTH REGULATOR FACTOR5 (GRF5), a transcriptional activator and key plant growth regulator, in Arabidopsis (Arabidopsis thaliana). Subsequently, GRF5 directly binds to the promoter of phyA (phytochrome A), encoding a far-red light (FR) sensor/cotyledon greening inhibitor. We demonstrate that the status of Glc within dark-grown etiolated cotyledons determines the de-etiolation of seedlings when exposed to light irradiation by the HXK1—GRF5—phyA molecular module. Thus, following seed germination, accumulating Glc within dark-grown etiolated cotyledons stimulates a HXK1-dependent increase of GRF5 and an associated decrease of phyA, triggering the perception, amplification and relay of HXK1-dependent Glc signaling, thereby facilitating the de-etiolation of seedlings following light irradiation. Our findings, therefore, establish how cotyledon carbohydrate signaling under subterranean darkness is sensed, amplified and relayed, determining the phase transition from skotomorphogenesis to photomorphogenesis on exposure to light irradiation.