UB2/UB3/TSH4-anchored transcriptional networks regulate early maize inflorescence development in response to simulated shade.

Increasing planting density has been adopted as an effective means to increase maize (Zea mays) yield. Competition for light from neighbors can trigger plant shade avoidance syndrome, which includes accelerated flowering. However, the regulatory networks of maize inflorescence development in response to high-density planting remain poorly understood. In this study, we showed that shade-mimicking treatments cause precocious development of the tassels and ears. Comparative transcriptome profiling analyses revealed the enrichment of phytohormone-related genes and transcriptional regulators among the genes co-regulated by developmental progression and simulated shade. Network analysis showed that three homologous Squamosa promoter binding protein (SBP)-like (SPL) transcription factors, Unbranched2 (UB2), Unbranched3 (UB3), and Tasselsheath4 (TSH4), individually exhibited connectivity to over 2,400 genes across the V3-to-V9 stages of tassel development. In addition, we showed that the ub2 ub3 double mutant and tsh4 single mutant were almost insensitive to simulated shade treatments. Moreover, we demonstrated that UB2/UB3/TSH4 could directly regulate the expression of Barren inflorescence2 (BIF2) and Zea mays teosinte branched1/cycloidea/proliferating cell factor30 (ZmTCP30). Furthermore, we functionally verified a role of ZmTCP30 in regulating tassel branching and ear development. Our results reveal a UB2/UB3/TSH4-anchored transcriptional regulatory network of maize inflorescence development and provide valuable targets for breeding shade-tolerant maize cultivars.

The evening complex promotes maize flowering and adaptation to temperate regions.

Maize (Zea mays) originated in southern Mexico and has spread over a wide latitudinal range. Maize expansion from tropical to temperate regions has necessitated a reduction of its photoperiod sensitivity. In this study, we cloned a quantitative trait locus (QTL) regulating flowering time in maize and show that the maize ortholog of Arabidopsis thaliana EARLY FLOWERING3, ZmELF3.1, is the causal locus. We demonstrate that ZmELF3.1 and ZmELF3.2 proteins can physically interact with ZmELF4.1/4.2 and ZmLUX1/2, to form evening complex(es; ECs) in the maize circadian clock. Loss-of-function mutants for ZmELF3.1/3.2 and ZmLUX1/2 exhibited delayed flowering under long-day and short-day conditions. We show that EC directly represses the expression of several flowering suppressor genes, such as the CONSTANS, CONSTANS-LIKE, TOC1 (CCT) genes ZmCCT9 and ZmCCT10, ZmCONSTANS-LIKE 3, and the PSEUDORESPONSE REGULATOR (PRR) genes ZmPRR37a and ZmPRR73, thus alleviating their inhibition, allowing florigen gene expression and promoting flowering. Further, we identify two closely linked retrotransposons located in the ZmELF3.1 promoter that regulate the expression levels of ZmELF3.1 and may have been positively selected during postdomestication spread of maize from tropical to temperate regions during the pre-Columbian era. These findings provide insights into circadian clock-mediated regulation of photoperiodic flowering in maize and new targets of genetic improvement for breeding.

ZmELF3.1 integrates the RA2-TSH4 module to repress maize tassel branching.

Tassel branch number (TBN) is a key agronomic trait for adapting to high-density planting and grain yield in maize. However, the molecular regulatory mechanisms underlying tassel branching are still largely unknown. Here, we used molecular and genetic studies together to show that ZmELF3.1 plays a critical role in regulating TBN in maize. Previous studies showed that ZmELF3.1 forms the evening complex through interacting with ZmELF4 and ZmLUX to regulate flowering in maize and that RA2 and TSH4 (ZmSBP2) suppresses and promotes TBN in maize, respectively. In this study, we show that loss-of-function mutants of ZmELF3.1 exhibit a significant increase of TBN. We also show that RA2 directly binds to the promoter of TSH4 and represses its expression, thus leading to reduced TBN. We further demonstrate that ZmELF3.1 directly interacts with both RA2 and ZmELF4.2 to form tri-protein complexes that further enhance the binding of RA2 to the promoter of TSH4, leading to suppressed TSH4 expression and consequently decreased TBN. Our combined results establish a novel functional link between the ELF3-ELF4-RA2 complex and miR156-SPL regulatory module in regulating tassel branching and provide a valuable target for genetic improvement of tassel branching in maize.

Local auxin biosynthesis regulates brace root angle and lodging resistance in maize.

Root lodging poses a major threat to maize production, resulting in reduced grain yield and quality, and increased harvest costs. Here, we combined expressional, genetic, and cytological studies to demonstrate a role of ZmYUC2 and ZmYUC4 in regulating gravitropic response of the brace root and lodging resistance in maize. We show that both ZmYUC2 and ZmYUC4 are preferentially expressed in root tips with partially overlapping expression patterns, and the protein products of ZmYUC2 and ZmYUC4 are localized in the cytoplasm and endoplasmic reticulum, respectively. The Zmyuc4 single mutant and Zmyuc2/4 double mutant exhibit enlarged brace root angle compared with the wild-type plants, with larger brace root angle being observed in the Zmyuc2/4 double mutant. Consistently, the brace root tips of the Zmyuc4 single mutant and Zmyuc2/4 double mutant accumulate less auxin and are defective in proper reallocation of auxin in response to gravi-stimuli. Furthermore, we show that the Zmyuc4 single mutant and the Zmyuc2/4 double mutant display obviously enhanced root lodging resistance. Our combined results demonstrate that ZmYUC2- and ZmYUC4-mediated local auxin biosynthesis is required for normal gravity response of the brace roots and provide effective targets for breeding root lodging resistant maize cultivars.

Transcription Factors FHY3 and FAR1 Regulate Light-Induced CIRCADIAN CLOCK ASSOCIATED1 Gene Expression in Arabidopsis.

The circadian clock provides a time-keeping mechanism that synchronizes various biological activities with the surrounding environment. Arabidopsis (Arabidopsis thaliana) CIRCADIAN CLOCK ASSOCIATED1 (CCA1), encoding a MYB-related transcription factor, is a key component of the core oscillator of the circadian clock, with peak expression in the morning. The molecular mechanisms regulating the light induction and rhythmic expression of CCA1 remain elusive. In this study, we show that two phytochrome signaling proteins, FAR-RED ELONGATED HYPOCOTYL3 (FHY3) and its paralog FAR-RED IMPAIRED RESPONSE1 (FAR1), are essential for the light-induced expression of CCA1 FHY3 and FAR1 directly bind to the CCA1 promoter and activate its expression, whereas PHYTOCHROME INTERACTING FACTOR5 (PIF5) directly binds to its promoter and represses its expression. Furthermore, PIF5 and TIMING OF CAB EXPRESSION1 physically interact with FHY3 and FAR1 to repress their transcriptional activation activity on CCA1 expression. These findings demonstrate that the photosensory-signaling pathway integrates with circadian oscillators to orchestrate clock gene expression. This mechanism might form the molecular basis of the regulation of the clock system by light in response to daily changes in the light environment, thus increasing plant fitness.

Arabidopsis FHY3 and FAR1 Regulate the Balance between Growth and Defense Responses under Shade Conditions.

Increasing crop yield per unit of area can be achieved by increasing planting density. However, high-density planting could trigger shade avoidance responses, which cause exaggerated growth and increased susceptibility to various diseases. Previous studies have shown that the rapid elongation of plants under shade (i.e., reduced red to far-red ratios) is regulated by phytochromes and various phytohormones. However, the detailed molecular mechanisms governing the interaction among these signaling pathways are not well understood. Here, we report that loss-of-function mutants of FAR-RED ELONGATED HYPOCOTYL3 (FHY3) and FAR-RED-IMPAIRED RESPONSE1 (FAR1), which encode two homologous transcription factors essential for phytochrome signaling, exhibit an exaggerated shade avoidance phenotype. We show that FHY3 and FAR1 repress plant growth through directly activating the expression of two atypical basic helix-loop-helix transcriptional cofactors, PHYTOCHROME RAPIDLY REGULATED1 (PAR1) and PAR2, and that this process is antagonized by a group of JASMONATE ZIM-DOMAIN proteins, key repressors of the jasmonic acid (JA) signaling pathway, through physical interactions. Furthermore, we show that FHY3 interacts with MYC2, a key transcriptional regulator of JA responses, coordinately regulating JA-responsive defense gene expression. Our results unveil a previously unrecognized mechanism whereby plants balance their growth and defense responses through convergence of the phytochrome signaling pathway and JA signaling pathway under shade conditions.

Characterization of Maize Phytochrome-Interacting Factors in Light Signaling and Photomorphogenesis.

Increasing planting density has been an effective means of increasing maize (Zea mays ssp. mays) yield per unit of land area over the past few decades. However, high-density planting will cause a reduction in the ratio of red to far-red incident light, which could trigger the shade avoidance syndrome and reduce yield. The molecular mechanisms regulating the shade avoidance syndrome are well established in Arabidopsis (Arabidopsis thaliana) but poorly understood in maize. Here, we conducted an initial functional characterization of the maize Phytochrome-Interacting Factor (PIF) gene family in regulating light signaling and photomorphogenesis. The maize genome contains seven distinct PIF genes, which could be grouped into three subfamilies: ZmPIF3s, ZmPIF4s, and ZmPIF5s Similar to the Arabidopsis PIFs, all ZmPIF proteins are exclusively localized to the nucleus and most of them can form nuclear bodies upon light irradiation. We show that all of the ZmPIF proteins could interact with ZmphyB. Heterologous expression of each ZmPIF member could partially or fully rescue the phenotype of the Arabidopsis pifq mutant, and some of these proteins conferred enhanced shade avoidance syndrome in Arabidopsis. Interestingly, all ZmPIF proteins expressed in Arabidopsis are much more stable than their Arabidopsis counterparts upon exposure to red light. Moreover, the Zmpif3, Zmpif4, and Zmpif5 knockout mutants generated via CRISPR/Cas9 technology all showed severely suppressed mesocotyl elongation in dark-grown seedlings and were less responsive to simulated shade treatment. Taken together, our results reveal both conserved and distinct molecular properties of ZmPIFs in regulating light signaling and photomorphogenesis in maize.

Light and Ethylene Coordinately Regulate the Phosphate Starvation Response through Transcriptional Regulation of PHOSPHATE STARVATION RESPONSE1.

Plants have evolved an array of adaptive responses to low Pi availability, a process modulated by various external stimuli and endogenous growth regulatory signals. Little is known about how these signaling processes interact to produce an integrated response. Arabidopsis thaliana PHOSPHATE STARVATION RESPONSE1 (PHR1) encodes a conserved MYB-type transcription factor that is essential for programming Pi starvation-induced gene expression and downstream Pi starvation responses (PSRs). Here, we show that loss-of-function mutations in FHY3 and FAR1, encoding two positive regulators of phytochrome signaling, and in EIN3, encoding a master regulator of ethylene responses, cause attenuated PHR1 expression, whereas mutation in HY5, encoding another positive regulator of light signaling, causes increased PHR1 expression. FHY3, FAR1, HY5, and EIN3 directly bind to the PHR1 promoter through distinct cis-elements. FHY3, FAR1, and EIN3 activate, while HY5 represses, PHR1 expression. FHY3 directly interacts with EIN3, and HY5 suppresses the transcriptional activation activity of FHY3 and EIN3 on PHR1 Finally, both light and ethylene promote FHY3 protein accumulation, and ethylene blocks the light-promoted stabilization of HY5. Our results suggest that light and ethylene coordinately regulate PHR1 expression and PSRs through signaling convergence at the PHR1 promoter.

ADF10 shapes the overall organization of apical actin filaments by promoting their turnover and ordering in pollen tubes.

Here, we show that Arabidopsis ADF10 plays an important role in shaping the overall organization of apical actin filaments by promoting their turnover and ordering. ADF10 severs and depolymerizes actin filaments in vitro and is distributed throughout the entire pollen tube. In adf10 mutants, severing and monomer dissociation events for apical actin filaments are reduced, and the apical actin structure extends further toward the tube base than in wild-type tubes. In particular, the percentage of apical actin filaments that form large angles to the tube growth axis is much higher in adf10 pollen tubes, and the actin filaments are more randomly distributed, implying that ADF10 promotes their ordering. Consistent with the role of apical actin filaments in physically restricting the movement of vesicles, the region in which apical vesicles accumulate is enlarged at the tip of adf10 pollen tubes. Both tipward and backward movements of small vesicles are altered within the growth domain of adf10 pollen tubes. Thus, our study suggests that ADF10 shapes the organization of apical actin filaments to regulate vesicle trafficking and pollen tube growth.

Exploiting SPL genes to improve maize plant architecture tailored for high-density planting.

Maize (Zea mays ssp. mays) is an agronomically important crop and also a classical genetic model for studying the regulation of plant architecture formation, which is a critical determinant of grain yield. Since the 1930s, increasing planting density has been a major contributing factor to the >7-fold increase in maize grain yield per unit land area in the USA, which is accompanied by breeding and utilization of cultivars characterized by high-density-tolerant plant architecture, including decreased ear height, lodging resistance, more upright leaves, reduced tassel branch number, and reduced anthesis-silking interval (ASI). Recent studies demonstrated that phytochrome-mediated red/far-red light signaling pathway and the miR156/SQUAMOSA-PROMOTER BINDING PROTEIN-LIKE (SPL) regulatory module co-ordinately regulate the shade avoidance response and diverse aspects of plant architecture in responding to shading in Arabidopsis. The maize genome contains 30 ZmSPL genes, and 18 of them are predicted as direct targets of zma-miR156s. Accumulating evidence indicates that ZmSPL genes play important roles in regulating maize flowering time, plant/ear height, tilling, leaf angle, tassel and ear architecture, and grain size and shape. Finally, we discuss ways to exploit maize SPL genes and downstream targets for improving maize plant architecture tailored for high-density planting.

VLN2 Regulates Plant Architecture by Affecting Microfilament Dynamics and Polar Auxin Transport in Rice.

As a fundamental and dynamic cytoskeleton network, microfilaments (MFs) are regulated by diverse actin binding proteins (ABPs). Villins are one type of ABPs belonging to the villin/gelsolin superfamily, and their function is poorly understood in monocotyledonous plants. Here, we report the isolation and characterization of a rice (Oryza sativa) mutant defective in VILLIN2 (VLN2), which exhibits malformed organs, including twisted roots and shoots at the seedling stage. Cellular examination revealed that the twisted phenotype of the vln2 mutant is mainly caused by asymmetrical expansion of cells on the opposite sides of an organ. VLN2 is preferentially expressed in growing tissues, consistent with a role in regulating cell expansion in developing organs. Biochemically, VLN2 exhibits conserved actin filament bundling, severing and capping activities in vitro, with bundling and stabilizing activity being confirmed in vivo. In line with these findings, the vln2 mutant plants exhibit a more dynamic actin cytoskeleton network than the wild type. We show that vln2 mutant plants exhibit a hypersensitive gravitropic response, faster recycling of PIN2 (an auxin efflux carrier), and altered auxin distribution. Together, our results demonstrate that VLN2 plays an important role in regulating plant architecture by modulating MF dynamics, recycling of PIN2, and polar auxin transport.

Arabidopsis actin-depolymerizing factor7 severs actin filaments and regulates actin cable turnover to promote normal pollen tube growth.

Actin filaments are often arranged into higher-order structures, such as the longitudinal actin cables that generate the reverse fountain cytoplasmic streaming pattern present in pollen tubes. While several actin binding proteins have been implicated in the generation of these cables, the mechanisms that regulate their dynamic turnover remain largely unknown. Here, we show that Arabidopsis thaliana actin-depolymerizing factor7 (ADF7) is required for turnover of longitudinal actin cables. In vitro biochemical analyses revealed that ADF7 is a typical ADF that prefers ADP-G-actin over ATP-G-actin. ADF7 inhibits nucleotide exchange on actin and severs filaments, but its filament severing and depolymerizing activities are less potent than those of the vegetative ADF1. ADF7 primarily decorates longitudinal actin cables in the shanks of pollen tubes. Consistent with this localization pattern, the severing frequency and depolymerization rate of filaments significantly decreased, while their maximum lifetime significantly increased, in adf7 pollen tube shanks. Furthermore, an ADF7-enhanced green fluorescent protein fusion with defective severing activity but normal G-actin binding activity could not complement adf7, providing compelling evidence that the severing activity of ADF7 is vital for its in vivo functions. These observations suggest that ADF7 evolved to promote turnover of longitudinal actin cables by severing actin filaments in pollen tubes.

Arabidopsis villins promote actin turnover at pollen tube tips and facilitate the construction of actin collars.

Apical actin filaments are crucial for pollen tube tip growth. However, the specific dynamic changes and regulatory mechanisms associated with actin filaments in the apical region remain largely unknown. Here, we have investigated the quantitative dynamic parameters that underlie actin filament growth and disappearance in the apical regions of pollen tubes and identified villin as the major player that drives rapid turnover of actin filaments in this region. Downregulation of Arabidopsis thaliana VILLIN2 (VLN2) and VLN5 led to accumulation of actin filaments at the pollen tube apex. Careful analysis of single filament dynamics showed that the severing frequency significantly decreased, and the lifetime significantly increased in vln2 vln5 pollen tubes. These results indicate that villin-mediated severing is critical for turnover and departure of actin filaments originating in the apical region. Consequently, the construction of actin collars was affected in vln2 vln5 pollen tubes. In addition to the decrease in severing frequency, actin filaments also became wavy and buckled in the apical cytoplasm of vln2 vln5 pollen tubes. These results suggest that villin confers rigidity upon actin filaments. Furthermore, an observed decrease in skewness of actin filaments in the subapical region of vln2 vln5 pollen tubes suggests that villin-mediated bundling activity may also play a role in the construction of actin collars. Thus, our data suggest that villins promote actin turnover at pollen tube tips and facilitate the construction of actin collars.

ZmGns, a maize class I ß-1,3-glucanase, is induced by biotic stresses and possesses strong antimicrobial activity.

Plant ß-1,3-glucanases are members of the pathogenesis-related protein 2 (PR-2) family, which is one of the 17 PR protein families and plays important roles in biotic and abiotic stress responses. One of the differentially expressed proteins (spot 842) identified in a recent proteomic comparison between five pairs of closely related maize (Zea mays L.) lines differing in aflatoxin resistance was further investigated in the present study. Here, the corresponding cDNA was cloned from maize and designated as ZmGns. ZmGns encodes a protein of 338 amino acids containing a potential signal peptide. The expression of ZmGns was detectible in all tissues studied with the highest level in silks. ZmGns was significantly induced by biotic stresses including three bacteria and the fungus Aspergillus flavus. ZmGns was also induced by most abiotic stresses tested and growth hormones including salicylic acid. In vivo, ZmGns showed a significant inhibitory activity against the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 and fungal pathogen Botrytis cinerea when it overexpressed in Arabidopsis. Its high level of expression in the silk tissue and its induced expression by phytohormone treatment, as well as by bacterial and fungal infections, suggest it plays a complex role in maize growth, development, and defense.

Oryza sativa actin-interacting protein 1 is required for rice growth by promoting actin turnover.

Rapid actin turnover is essential for numerous actin-based processes. However, how it is precisely regulated remains poorly understood. Actin-interacting protein 1 (AIP1) has been shown to be an important factor by acting coordinately with actin-depolymerizing factor (ADF)/cofilin in promoting actin depolymerization, the rate-limiting factor in actin turnover. However, the molecular mechanism by which AIP1 promotes actin turnover remains largely unknown in plants. Here, we provide a demonstration that AIP1 promotes actin turnover, which is required for optimal growth of rice plants. Specific down-regulation of OsAIP1 increased the level of filamentous actin and reduced actin turnover, whereas over-expression of OsAIP1 induced fragmentation and depolymerization of actin filaments and enhanced actin turnover. In vitro biochemical characterization showed that, although OsAIP1 alone does not affect actin dynamics, it enhances ADF-mediated actin depolymerization. It also caps the filament barbed end in the presence of ADF, but the capping activity is not required for their coordinated action. Real-time visualization of single filament dynamics showed that OsAIP1 enhanced ADF-mediated severing and dissociation of pointed end subunits. Consistent with this, the filament severing frequency and subunit off-rate were enhanced in OsAIP1 over-expressors but decreased in RNAi protoplasts. Importantly, OsAIP1 acts coordinately with ADF and profilin to induce massive net actin depolymerization, indicating that AIP1 plays a major role in the turnover of actin, which is required to optimize F-actin levels in plants.

Arabidopsis VILLIN5, an actin filament bundling and severing protein, is necessary for normal pollen tube growth.

A dynamic actin cytoskeleton is essential for pollen germination and tube growth. However, the molecular mechanisms underlying the organization and turnover of the actin cytoskeleton in pollen remain poorly understood. Villin plays a key role in the formation of higher-order structures from actin filaments and in the regulation of actin dynamics in eukaryotic cells. It belongs to the villin/gelsolin/fragmin superfamily of actin binding proteins and is composed of six gelsolin-homology domains at its core and a villin headpiece domain at its C terminus. Recently, several villin family members from plants have been shown to sever, cap, and bundle actin filaments in vitro. Here, we characterized a villin isovariant, Arabidopsis thaliana VILLIN5 (VLN5), that is highly and preferentially expressed in pollen. VLN5 loss-of-function retarded pollen tube growth and sensitized actin filaments in pollen grains and tubes to latrunculin B. In vitro biochemical analyses revealed that VLN5 is a typical member of the villin family and retains a full suite of activities, including barbed-end capping, filament bundling, and calcium-dependent severing. The severing activity was confirmed with time-lapse evanescent wave microscopy of individual actin filaments in vitro. We propose that VLN5 is a major regulator of actin filament stability and turnover that functions in concert with oscillatory calcium gradients in pollen and therefore plays an integral role in pollen germination and tube growth.

High temperature inhibits vascular development via the PIF4-miR166-HB15 module in Arabidopsis.

The plant vascular system is an elaborate network of conducting and supporting tissues that extends throughout the plant body, and its structure and function must be orchestrated with different environmental conditions. Under high temperature, plants display thin and lodging stems that may lead to decreased yield and quality of crops. However, the molecular mechanism underlying high-temperature-mediated regulation of vascular development is not known. Here, we show that Arabidopsis plants overexpressing the basic-helix-loop-helix (bHLH) transcription factor PHYTOCHROME INTERACTING FACTOR 4 (PIF4), a central regulator of high-temperature signaling, display fewer vascular bundles (VBs) and decreased secondary cell wall (SCW) thickening, mimicking the lodging inflorescence stems of high-temperature-grown wild-type plants. Rising temperature and elevated PIF4 expression reduced the expression of MIR166 and, concomitantly, elevated the expression of the downstream class III homeodomain leucine-zipper (HD-ZIP III) family gene HB15. Consistently, knockdown of miR166 and overexpression of HB15 led to inhibition of vascular development and SCW formation, whereas the hb15 mutant displayed the opposite phenotype in response to high temperature. Moreover, in vitro and in vivo assays verified that PIF4 binds to the promoters of several MIR166 genes and represses their expression. Our study establishes a direct functional link between PIF4 and the miR166-HB15 module in modulating vascular development and SCW thickening and consequently stem-lodging susceptibility at elevated temperatures.

Treatment and diagnosis of hyperlipidemia acute pancreatitis in pregnancy associated with pre­pregnancy obesity and diabetes: A case report.

Hyperlipidemia acute pancreatitis (HLAP) is a specific type of pancreatitis mainly caused by elevated serum triglyceride (TG) levels. Therefore, knowledge of patients' medical history is crucial to the identification of those at high risk of HLAP. Diabetes and obesity are associated with high levels of triglycerides, a risk factor for the development of HLAP, which should be controlled before pregnancy. Moreover, HLAP is associated with additional diagnostic and management challenges related to hyperlipidemia (HL) and pregnancy. HLAP during pregnancy has a rapid onset and rapid progression, and complications are more likely to damage the function of multiple organs. HLAP is more common after 28 weeks of pregnancy, the cause is mostly high TG and the serum TG of the patient is often >1,000 mg/d1. Clinicians should be alert to the occurrence of server acute pancreatitis (AP). Therefore, clinicians need to identify and implement effective treatment in a timely manner to control the progression of HLAP during pregnancy and improve pregnancy outcomes. The present study reported the case of a 26-year-old pregnant patient who was hospitalized for epigastric pain at 35 weeks and 2 days of gestation. Medical and family history reported previous diagnoses of diabetes and obesity (weight before pregnancy, 103 kg; BMI, 36.40 kg/m2). Laboratory tests demonstrated high levels of lipase and amylase, a notable systemic inflammatory response, HL, coagulopathy, hypoproteinemia and hyperglycemia. Abdominal ultrasonography demonstrated a hypoechoic pancreatic head. A clinical diagnosis of AP was confirmed using CT scanning. Initial interventions for HLAP included aggressive intravenous hydration, bowel rest, pain control and a combination of heparin and insulin. Lipid-lowering agents were administered to reduce serum lipid levels. Hemoperfusion and continuous renal replacement therapy were also used to rapidly counteract the elevated lipid levels. Antibiotics were administered in the present case because inflammatory markers such as leukocytes, neutrophils and C-reactive protein were elevated. The patient and newborn were discharged 11 days after hospitalization, with an improvement in maternal clinical health and the infant was healthy. When evaluating pregnant patients with pre-obesity and diabetes presenting with abdominal pain, obstetricians should consider HLAP. Timely diagnosis and multi-team precision treatment are effective for good outcomes for mother and baby.

Arabidopsis FHY3 and FAR1 Function in Age Gating of Leaf Senescence.

Leaf senescence is the terminal stage of leaf development. Both light and the plant hormone ethylene play important roles in regulating leaf senescence. However, how they coordinately regulate leaf senescence during leaf development remains largely unclear. In this study, we show that FHY3 and FAR1, two homologous proteins essential for phytochrome A-mediated light signaling, physically interact with and repress the DNA binding activity of EIN3 (a key transcription factor essential for ethylene signaling) and PIF5 (a bHLH transcription factor negatively regulating light signaling), and interfere with their DNA binding to the promoter of ORE1, which encodes a key NAC transcription factor promoting leaf senescence. In addition, we show that FHY3, PIF5, and EIN3 form a tri-protein complex(es) and that they coordinately regulate the progression of leaf senescence. We show that during aging or under dark conditions, accumulation of FHY3 protein decreases, thus lifting its repression on DNA binding of EIN3 and PIF5, leading to the increase of ORE1 expression and onset of leaf senescence. Our combined results suggest that FHY3 and FAR1 act in an age gating mechanism to prevent precocious leaf senescence by integrating light and ethylene signaling with developmental aging.