New insights into plant nutrient signaling and adaptation to fluctuating environments

Over the past 50 years, the Green Revolution and exploitation of heterosis have allowed cereal grain yield to keep pace with world- wide population growth. Unfortunately, plant growth and crop productivity are heavily dependent on the application of synthetic fertilizers.

Nutrient mTORC1 signaling contributes to hepatic lipid metabolism in the pathogenesis of non-alcoholic fatty liver disease

Energy metabolism is maintained by the complex homeostatic system in multiple cells and organs involving“nutrient signaling”or“nutrient sensor”.Overnutrient-induced chronic metabolic diseases,as the hallmarks of the 21st century’s public health,are growing threat worldwide.In the past two decades,non-alcoholic fatty liver disease(NAFLD)has emerged as the most prevalent form of chronic liver dis-ease,affecting globally,and increases the risk of incident obesity,type 2 diabetes,and insulin resistance.NAFLD begins with the excessive triglyceride accumulation in hepatocytes,and develops to hepatocel-lular steatosis with inflammation(non-alcoholic steatohepatitis,NASH),fibrosis,cirrhosis,and ultimately hepatocellular carcinoma(HCC).The liver is the central mediator of lipid metabolism by regulation of fatty acid(FA)uptake,manufacture,store,export,and oxidation in response to physiological fluctuations of nutrient.Sterol regulatory element-binding protein c(SREBP-1c)-mediated de novo lipogenesis(DNL)is an important nutritional regulator in biosynthesis of FAs and triglyceride in the liver.Mechanistic target of rapamycin complex 1(mTORC1),as a central hub of nutrient signaling,controls cellular metabolism and growth mainly via increasing anabolic processes and inhibiting catabolic processes in response to physiological fluctuations of nutrient.mTORC1 activation contributes to regulation of DNL by increasing SREBP1 transcription,which contributes to NAFLD pathogenesis and accelerates NAFLD-related HCC development.In this review,we provide the comprehensive understanding of the molec-ular mechanism of SREBPs and autophagy to control hepatic lipid homeostasis under nutrient availability in physiological and pathophysiological states,and highlight how nutrient mTORC1 signaling coordi-nately to integrate the lipid metabolic regulation and therapeutic targets in NAFLD and HCC.

Plant mineral nutrient sensing and signaling

As terrestrial plants are sessile organisms and therefore must directly deal with an often complex and changing environment, they have had to develop complex and elegant strategies to survive and thrive in the face of environmental stress. This is particularly true for plant adaptation to the soil environment, where essential mineral nutrients often are found at sub- optimal levels and their concentrations can vary significantly, both spatially and temporally. Furthermore, plants also at times have to respond to excessively high and potentially toxic levels of essential nutrients, as well as toxic levels of non- essential metals and metalloids in the soil. Although plant mineral nutrition as a bona ~ide research discipline has a history of over 15o years, beginning with the pioneering work of Justus Von Liebieg and others in the mid-1800＇s, it is only very recently that researchers have begun to truly appreciate how sophisticated plants are with regards to the sensing of their mineral status and the maintaining of mineral homeostasis in the plant.

Nutrient-hormone relations:Driving root plasticity in plants

Optimal plant development requires root uptake of 14 essential mineral elements from the soil.Since the bioavailability of these nutrients underlies large variation in space and time,plants must dynamically adjust their root architecture to optimize nutrient access and acquisition.The information on external nutrient availability and whole-plant demand is translated into cellular signals that often involve phytohormones as intermediates to trigger a systemic or locally restricted developmental response.Timing and extent of such local root responses depend on the overall nutritional status of the plant that is transmitted from shoots to roots in the form of phytohormones or other systemic long-distance signals.The integration of these systemic and local signals then determines cell division or elongation rates in primary and lateral roots,the initiation,emergence,or elongation of lateral roots,as well as the formation of root hairs.Here,we review the cascades of nutrient-related sensing and signaling events that involve hormones and highlight nutrient-hormone relations that coordinate root developmental plasticity in plants.

Autophagy and the nutritional signaling pathway

During their growth and development, animals adapt to tremendous changes in order to survive. These include responses to both environmental and physiological changes and autophagy is one of most important adaptive and regulatory mechanisms. Autophagy is defined as an autolytic process to clear damaged cellular organelles and recycle the nutrients via lysosomic degradation. The process of autophagy responds to special conditions such as nutrient withdrawal. Once autophagy is induced,phagophores form and then elongate and curve to form autophagosomes. Autophagosomes then engulf cargo,fuse with endosomes, and finally fuse with lysosomes for maturation. During the initiation process, the ATG1/ULK1(unc-51-like kinase 1) and VPS34(which encodes a class III phosphatidylinositol(Ptd Ins) 3-kinase) complexes are critical in recruitment and assembly of other complexes required for autophagy. The process of autophagy is regulated by autophagy related genes(ATGs). Amino acid and energy starvation mediate autophagy by activating m TORC1(mammalian target of rapamycin) and AMPactivated protein kinase(AMPK). AMPK is the energy status sensor, the core nutrient signaling component and the metabolic kinase of cells. This review mainly focuses on the mechanism of autophagy regulated by nutrient signaling especially for the two important complexes,ULK1 and VPS34.