SHORT-ROOT Stabilizes PHOSPHATE1 to Regulate Phosphate Allocation in Arabidopsis

Coordinated distribution of Pi between roots and shoots is an important process that plants use to maintain Pi homeostasis. SHR (SHORT-ROOT) is well-characterized for its function in root radial patterning1-3. Here, we demonstrate a new role of SHR in controlling phosphate (Pi) allocation from roots to shoots by regulating PHOSPHATE1 (PHO1) in the root differentiation zone. We recovered a weak mutant allele of SHR in Arabidopsis which accumulates much less Pi in the shoot and shows constitutive Pi starvation response (PSR) under Pi-sufficient condition. Besides, Pi starvation suppresses SHR protein accumulation and releases its inhibition on the HD-ZIP Ⅲ transcription factor PHB. PHB accumulates and directly binds the promoter of PHO2 to upregulate its transcription, resulting in PHO1 degradation in the xylem-pole pericycle cells. Our findings reveal a previously unrecognized mechanism of how plants repress Pi translocation from roots to shoots in response to Pi starvation.

Polyphosphate affects cytoplasmic and chromosomal dynamics in nitrogen-starved Pseudomonas aeruginosa

Polyphosphate (polyP) synthesis is a ubiquitous stress and starvation response in bacteria. In diverse species, mutants unable to make polyP have a wide variety of physiological defects, but the mechanisms by which this simple polyanion exerts its effects remain unclear. One possibility is that polyP′s many functions stem from global effects on the biophysical properties of the cell. We characterize the effect of polyphosphate on cytoplasmic mobility under nitrogen-starvation conditions in the opportunistic pathogen Pseudomonas aeruginosa. Using fluorescence microscopy and particle tracking, we characterize the motion of chromosomal loci and free tracer particles in the cytoplasm. In the absence of polyP and upon starvation, we observe an increase in mobility both for chromosomal loci and for tracer particles. Tracer particles reveal that polyP also modulates the partitioning between a ′more mobile′ and a ′less mobile′ population: small particles in cells unable to make polyP are more likely to be ′mobile′ and explore more of the cytoplasm, particularly during starvation. We speculate that this larger freedom of motion may be a consequence of nucleoid decompaction, which we also observe in starved cells deficient in polyP. Our observations suggest that polyP limits cytoplasmic mobility and accessibility during nitrogen starvation, which may help to explain the pleiotropic phenotypes observed in the absence of polyP.

Formimidoyltransferase cyclodeaminase prevents the starvation-induced liver hepatomegaly and dysfunction through downregulating mTORC1

The liver is a crucial center in the regulation of energy homeostasis under starvation. Although downregulation of mammalian target of rapamycin complex 1 (mTORC1) has been reported to play pivotal roles in the starvation responses, the underpinning mechanisms in particular upstream factors that downregulate mTORC1 remain largely unknown. To identify genetic variants that cause liver energy disorders during starvation, we conduct a zebrafish forward genetic screen. We identify a liver hulk (lvh) mutant with normal liver under feeding, but exhibiting liver hypertrophy under fasting. The hepatomegaly in lvh is caused by enlarged hepatocyte size and leads to liver dysfunction as well as limited tolerance to starvation. Positional cloning reveals that lvh phenotypes are caused by mutation in the ftcd gene, which encodes the formimidoyltransferase cyclodeaminase (FTCD). Further studies show that in response to starvation, the phosphorylated ribosomal S6 protein (p-RS6), a downstream effector of mTORC1, becomes downregulated in the wild-type liver, but remains at high level in lvh. Inhibition of mTORC1 by rapamycin rescues the hepatomegaly and liver dysfunction of lvh. Thus, we characterize the roles of FTCD in starvation response, which acts as an important upstream factor to downregulate mTORC1, thus preventing liver hypertrophy and dysfunction.

Unraveling a Bacterial Starvation Response Through the Direct Targets of a Starvation-Induced Transcriptional Activator

Organisms frequently encounter environments with nutrient shortages and their survival depends on changes in physiology and the ability to conserve resources. In bacteria, many physiological changes associated with starvation have been identified, but the underlying genetic components and regulatory networks that direct these physiological changes are often poorly defined. Here, we aimed to better define the gene regulatory networks that mediate the starvation response in Myxococcus xanthus, a bacterium that copes with starvation by producing fruiting bodies filled with dormant and stress-resistant spores. We focused on the direct promoter/gene targets of Nla28, a transcriptional activator/enhancer binding protein (EBP) that is important for early rounds of gene expression following starvation. Using expression profiling to identify genes that are downregulated in nla28 mutant cells and bioinformatics to identify the putative promoters of these genes, 12 potential promoter targets (37 genes) of Nla28 were identified. The results of in vitro promoter binding assays, coupled with in vitro and in vivo mutational analyses, suggested that the 12 promoters are in vivo targets of Nla28 and that Nla28 dimers use tandem, imperfect repeats of an 8-bp sequence for binding. Interestingly, nine of the Nla28 target promoters are intragenic, located in the protein coding sequence of an upstream gene or in the protein coding sequence of one gene within an operon (internal promoters). Based on mutational analyses, we concluded that the 12 Nla28 target loci contain at least one gene important for production of stress-resistant spores following starvation. Most of these loci contain genes predicted to be involved in regulatory or defense-related functions. Using the consensus Nla28 binding sequence, followed by bioinformatics and expression profiling, 58 additional promoters and 102 genes were tagged as potential Nla28 targets. Among these putative Nla28 targets, functions such as regulatory, metabolic and cell envelope biogenesis were commonly assigned to genes.

Maternal starvation primes progeny response to nutritional stress

Organisms adapt to environmental changes in order to survive. Mothers exposed to nutritional stresses can induce an adaptive response in their offspring. However, the molecular mechanisms behind such inheritable links are not clear. Here we report that in Drosophila, starvation of mothers primes the progeny against subsequent nutritional stress. We found that RpL10Ab represses TOR pathway activity by genetically interacting with TOR pathway components TSC2 and Rheb. In addition, starved mothers produce offspring with lower levels of RpL10Ab in the germline, which results in higher TOR pathway activity, conferring greater resistance to starvation-induced oocyte loss. The RpL10Ab locus encodes for the RpL10Ab mRNA and a stable intronic sequence RNA (sisR-8), which collectively repress RpL10Ab pre-mRNA splicing in a negative feedback mechanism. During starvation, an increase in maternally deposited RpL10Ab and sisR-8 transcripts leads to the reduction of RpL10Ab expression in the offspring. Our study suggests that the maternally deposited RpL10Ab and sisR-8 transcripts trigger a negative feedback loop that mediates intergenerational adaptation to nutritional stress as a starvation response.

PHOSPHATE STARVATION RESPONSE enables arbuscular mycorrhiza symbiosis

Arbuscular mycorrhiza (AM) is a widespread symbiosis between roots of the majority of land plants and Glomeromycotina fungi. AM is important for ecosystem health and functioning as the fungi critically support plant performance by providing essential mineral nutrients, particularly the poorly accessible phosphate, in exchange for organic carbon. AM fungi colonize the inside of roots and this is promoted at low but inhibited at high plant phosphate status, while the mechanistic basis for this phosphate-dependence remained obscure. Here we demonstrate that a major transcriptional regulator of phosphate starvation responses in rice PHOSPHATE STARVATION RESPONSE 2 (PHR2) regulates AM. Root colonization of phr2 mutants is drastically reduced, and PHR2 is required for root colonization, mycorrhizal phosphate uptake, and yield increase in field soil. PHR2 promotes AM by targeting genes required for pre-contact signaling, root colonization, and AM function. Thus, this important symbiosis is directly wired to the PHR2-controlled plant phosphate starvation response.