Biology subjects

Wang, X.-F.

Publications and source records attributed to Wang, X.-F..

18 recordsLinked to original sources

bioRxiv2026

Leptin Acts as a Peripheral Tropic Signal to Tune Steroidogenesis

The integration of metabolic status with reproductive and developmental timing is a cornerstone of animal physiology, yet how steroidogenesis rapidly adapts to abrupt environmental changes remains poorly understood. Here, we identify a peptide hormone circuit in which leptin or its analogs act as peripheral tropic signals, directly coupling systemic metabolic state to steroid hormone production through dynamic remodeling of intracellular lipid pools. Mechanistically, spatiotemporal fluctuations in leptin activate JAK/STAT signaling within steroidogenic tissues to reprogram the balance among lipid droplets, cholesteryl esters, and free cholesterol, thereby tuning the amplitude and timing of steroid hormone pulses via hormone-sensitive lipase (Hsl), a rate-limiting determinant of steroidogenic flux. Cross-species analyses in Drosophila melanogaster, Blattella germanica, and Mus musculus suggest a partially conserved leptin-JAK/STAT-lipase axis that functions as a metabolic "sterol rheostat", enabling rapid modulation of steroidogenesis in response to systemic metabolic and stress cues. These findings reveal a metabolic-endocrine mechanism by which leptin can act directly on steroidogenic organs to regulate hormonal output.

developmental biology↗

bioRxiv2025

Polyploidy promotes transformation of epithelial cells into non-professional phagocytes

Removal of dead and damaged cells is critical for organismal health. Under stress conditions such as nutritional deprivation, infection, or temperature shift, the clearance of nonessential cells becomes a universal strategy to conserve energy and maintain tissue homeostasis. Typically, this task is performed by professional phagocytes such as macrophages. However, non-professional phagocytes (NPPs) can also adopt a phagocytic fate under specific circumstances. Similar to professional phagocytes, NPPs undergo transitions from immature to mature states and activation, but the precise cellular and molecular mechanisms governing their maturation, induction and phagocytic execution remain largely unknown. A notable example of stress-induced phagocytosis is the removal of germline cells by follicle cell-derived NPPs during oogenesis in Drosophila. In this study, we report that the transformation of follicle cells into NPPs is dependent on Notch signaling activation during mid-oogenesis. Moreover, Notch overactivation is sufficient to trigger germline cell death and clearance (GDAC). We further show that polyploidy, driven by Notch signaling-induced endoreplication, is essential for the transformation of follicle cells into NPPs. Polyploidy facilitates the activation of JNK signaling, which is crucial for the phagocytic behavior of these cells. Additionally, we show that polyploidy in epidermal cells, another type of NPPs, is important for their engulfment of dendrites during induced degeneration. Together, these findings suggest that polyploidy is a critical factor in the transformation of epithelial cells into NPPs, enabling their phagocytic functions, which are essential for maintaining cellular and organismal homeostasis during stress conditions. SIGNIFICANCEThe ability to remove dead and damaged cells is essential for maintaining tissue homeostasis and organismal health. While this task is typically performed by professional phagocytes such as macrophages, non-professional phagocytes (NPPs) can also acquire phagocytic functions during development or in response to stress conditions. Using Drosophila oogenesis as a model, we reveal that the transformation of follicle cells into NPPs is driven by Notch signaling and is critically dependent on polyploidy. Our findings show that polyploidy, induced through Notch signaling-mediated endoreplication, is required for activating JNK signaling, a pathway essential for the phagocytic behavior of NPPs. Furthermore, we show that polyploidy also facilitates the phagocytic activity of epidermal cells in clearing degenerating dendrites. Together, these results suggest that polyploidy plays an important role in enabling epithelial cells to adopt NPP functions and in maintaining tissue and organismal homeostasis under stress conditions.

developmental biology↗

bioRxiv2025

Functional redundancy in chicken ANP32A mediates species-specific support of avian influenza virus polymerase

Host restriction of avian influenza virus (AIV) polymerase in human cells is driven by species-specific differences in ANP32A/B proteins. While AIV polymerase relies on ANP32A/B containing a 33-amino-acid insert unique to avian species, the structural and/or mechanistic basis for this requirement remains poorly characterized. Here, we demonstrate that chicken ANP32A (chANP32A) displays three functional determinants enabling its species-specific support of AIV polymerase: (1) a SUMO-interacting motif (SIM), (2) SUMOylation at residues K68/K153, and (3) a 28-amino-acid segment within the avian-specific insertion. These determinants function synergistically and redundantly, requiring at least two for optimal activity, to enhance interactions between AIV viral ribonucleoprotein (vRNP) and chANP32A, thereby promoting AIV vRNP assembly. In contrast, human ANP32A/B--which lack the other two determinants and rely solely on SUMOylation--exhibit a limited capacity to support AIV polymerase activity. Our findings unveil a cooperative mechanism where SUMO-dependent processes and structural motifs in chANP32A enforce species-specific adaptation of AIV polymerase, shedding light on how ANP32A/B governs host restriction of AIV polymerase.

microbiology↗

bioRxiv2025

Amyloid-β precursor protein promotes tumor growth by establishing an immune-exclusive tumor microenvironment

During initiation and progression, cancerous tissue hijacks a series of elaborate tissue homeostatic mechanisms to avoid immune surveillance, including neuro-immune interactions. Here, we show that amyloid-{beta} precursor protein (APP) and its {beta}-cleavage product amyloid-{beta}1-42 (A{beta}1-42), well-known in the pathogenesis of Alzheimers disease (AD), are expressed in multiple cancer tissues. However, the oncogenic activity of APP is due to its E1 domain, instead of A{beta}1-42. Mechanistically, APP restricts immune cells influx into tumor microenvironment (TME) and impairs CD8+ T cell and NK cell-based immunity, by dampening type I interferon (IFN) response in TME. We also provide proof-of-concept that vaccination targeting APP is effective for cancer prevention. Our current study reveals a previously unrecognized role of APP in cancer immune surveillance, and provides a new strategy for cancer prevention and treatment by targeting APP.

cancer biology↗

bioRxiv2025

Neoadjuvant anti-4-1BB confers protection against spontaneous metastasis through low-affinity intratumor CD8+ T cells in triple-negative breast cancer

Neoadjuvant immunotherapy seeks to harness the primary tumor as a source of relevant tumor antigens to enhance systemic anti-tumor immunity through improved immunological surveillance. Despite having revolutionized the treatment of patients with high-risk early-stage triple-negative breast cancer (TNBC), a significant portion of patients remain unresponsive and succumb to metastatic recurrence post-treatment. Here, we found that optimally scheduled neoadjuvant administration of anti-4-1BB monotherapy was able to counteract metastases and prolong survival following surgical resection. Phenotypic and transcriptional profiling revealed enhanced 4-1BB expression on tumor-infiltrating intermediate (Tint), relative to progenitor (Tprog) and terminally exhausted (Tterm) T cells. Furthermore, Tint was enriched in low-affinity T cells. Treatment with anti-4-1BB drove clonal expansion of Tint, with reduced expression of tissue-retention marker CD103 in Tprog. This was accompanied by increased TCR clonotype sharing between paired tumors and pre-metastatic lungs. Further interrogation of sorted intratumor T cells confirmed enhanced T cell egress into circulation following anti-4-1BB treatment. In addition, gene signature extracted from anti-4-1BB treated Tint was consistently associated with improved clinical outcomes in BRCA patients. Combinatorial neoadjuvant anti-4-1BB and ablation of tumor-derived CXCL16 resulted in enhanced therapeutic effect. These findings illustrate the intratumor changes underpinning the efficacy of neoadjuvant anti-4-1BB, highlighting the reciprocity between local tissue-retention and distant immunologic fortification, suggesting treatment can reverse the siphoning of intratumor T cells to primary tumor, enabling redistribution to distant tissues and subsequent protection against metastases.

immunology↗

bioRxiv2024

Human ANP32A/B are SUMOylated and utilized by avian influenza virus NS2 protein to overcome species-specific restriction

Human ANP32A/B (huANP32A/B) poorly support the polymerase activity of avian influenza viruses (AIVs), thereby limiting interspecies transmission of AIVs from birds to humans. The SUMO-interacting motif (SIM) within NS2 promotes the adaptation of AIV polymerase to huANP32A/B via a yet undisclosed mechanism. Here we show that huANP32A/B are SUMOylated by the E3 SUMO ligase PIAS2, and deSUMOylated by SENP1. SUMO modification of huANP32A/B results in the recruitment of NS2, thereby facilitating huANP32A/B-supported AIV polymerase activity. Such a SUMO-dependent recruitment of NS2 is mediated by its association with huANP32A/B via the SIM-SUMO interaction module, where K68/K153-SUMO in huANP32A or K68/K116-SUMO in huANP32B interacts with the NS2-SIM. The SIM-SUMO interactions between huANP32A/B and NS2 function to promote AIV polymerase activity by positively regulating AIV vRNP-huANP32A/B interactions and AIV vRNP assembly. Our study offers insights into the mechanism of NS2 SIM in facilitating AIVs adaptation to mammals.

microbiology↗

bioRxiv2024

ProT-Diff: A Modularized and Efficient Approach to De Novo Generation of Antimicrobial Peptide Sequences through Integration of Protein Language Model and Diffusion Model

Antimicrobial Peptides (AMPs) represent a promising class of antimicrobial agents crucial for combating antibiotic-resistant pathogens. Despite the emergence of deep learning approaches for AMP discovery, there remains a gap in efficiently generating novel AMPs across various amino acid lengths without prior knowledge of peptide structures or sequence alignments. Here we introduce ProT-Diff, a modularized and efficient deep generative approach that ingeniously combines a pre-trained protein language model with a diffusion model to de novo generate candidate AMP sequences. ProT-Diff enabled the rapid generation of thousands of AMPs with diverse lengths within hours. Following in silico screening based on physicochemical properties and predicted antimicrobial activities, we selected 35 peptides for experimental validation. Remarkably, 34 of these peptides demonstrated antimicrobial activity against Gram-positive or Gram-negative bacteria, with 6 exhibiting broad-spectrum efficacy. Of particular interest, AMP_2, one of the broad-spectrum peptides, displayed potent antimicrobial activity, low hemolysis, and minimal cytotoxicity. Further in vivo assessment revealed its high effectiveness against a clinically relevant drug-resistant E. coli strain in a mouse model of acute peritonitis. This study not only presents a viable generative strategy for novel AMP design but also underscores its potential for generating other functional peptides, thereby broadening the horizon for new drug development.

synthetic biology↗

bioRxiv2023

Neuronal connectivity, behavioral, and transcriptional alterations associated with the loss of MARK2

Neuronal connectivity is essential for adaptive brain responses and can be modulated by dendritic spine plasticity and the intrinsic excitability of individual neurons. Dysregulation of these processes can lead to aberrant neuronal activity, which has been associated with numerous neurological disorders including autism, epilepsy, and Alzheimers disease. Nonetheless, the molecular mechanisms underlying aberrant neuronal connectivity remains unclear. We previously found that the serine/threonine kinase Microtubule Affinity Regulating Kinase 2 (MARK2), also known as Partitioning Defective 1b (Par1b), is important for the formation of dendritic spines in vitro. However, despite its genetic association with several neurological disorders, the in vivo impact of MARK2 on neuronal connectivity and cognitive functions remains unclear. Here, we demonstrate that loss of MARK2 in vivo results in changes to dendritic spine morphology, which in turn leads to a decrease in excitatory synaptic transmission. Additionally, loss of MARK2 produces substantial impairments in learning and memory, anxiety, and social behavior. Notably, MARK2 deficiency results in heightened seizure susceptibility. Consistent with this observation, RNAseq analysis reveals transcriptional changes in genes regulating synaptic transmission and ion homeostasis. These findings underscore the in vivo role of MARK2 in governing synaptic connectivity, cognitive functions, and seizure susceptibility.

neuroscience↗

bioRxiv2022

Cell polarity opposes Jak-STAT mediated Escargot activation that drives intratumor heterogeneity in a Drosophila tumor model

In proliferating neoplasms, microenvironment-derived selective pressures promote tumor heterogeneity by imparting diverse capacities for growth, differentiation and invasion. However, what makes a tumor cell respond to signaling cues differently from a normal cell is not well understood. In the Drosophila ovarian follicle cells, apicobasal-polarity loss induces heterogenous epithelial multilayering. When exacerbated by oncogenic-Notch expression, this multilayer displays an increased consistency in the occurrence of morphologically distinguishable cells adjacent to the polar follicle cells. Polar cells release the Jak-STAT ligand Unpaired (Upd), in response to which, neighboring polarity-deficient cells exhibit a precursor-like transcriptomic state. Using single-cell transcriptomics, we discovered the ectopic activation of the Snail-family transcription factor Escargot (Esg) in these cells. We also characterized similar relationship between Upd and Esg during early follicular development, where the establishment of polarity determines follicle-cell differentiation. Overall, our results indicate that epithelial-cell polarity acts as a gatekeeper against microenvironmental selective pressures that drive heterogeneity.

cancer biology↗

bioRxiv2022

Single-cell transcriptomics identifies regulation of invasive behavior in Drosophila follicle cells with polarity loss

Apicobasal cell-polarity loss is a founding event in Epithelial-Mesenchymal Transition (EMT) and epithelial tumorigenesis, yet how pathological polarity loss induces plasticity changes remains largely unknown. To understand the mechanisms and mediators regulating plasticity upon polarity loss, we performed single-cell (sc) RNA sequencing of Drosophila ovaries, where inducing polarity-gene l(2)gl knockdown (Lgl-KD) causes invasive delamination of the follicular epithelia. Integrating Lgl-KD with the corresponding wild-type sc-transcriptome, we discovered clusters specific to various discernible phenotype-specific cell types and further characterized the regulons active in those cells. A genetic requirement of Keap1-Nrf2 signaling in promoting multilayer formation of Lgl-KD cells was further identified. Elevated expression of Keap1 increased the volume of delaminated follicle cells that undergo enhanced collective invasion via cytoskeletal remodeling. Overall, our findings describe the comprehensive transcriptome of the follicle-cell tumor model at the single-cell resolution and identify a previously unappreciated link between stress signaling and cell plasticity in early tumorigenesis.

developmental biology↗

bioRxiv2022

A novel fully-spliced accessory gene in equine lentivirus with distinct Rev-responsive element

All lentiviruses encode an accessory protein Rev, whose main biological function is to mediate the nuclear export of unspliced and incompletely spliced viral transcripts by binding to a viral cis-acting element (termed the Rev-responsive element, RRE) that is located within env-encoding region. Equine infectious anemia virus (EIAV) is a member of the Lentivirus genus in the Retroviridae family, and is considered an important model for the study of lentivirus pathogenesis. Here, we identified a novel transcript from the EIAV genome that encodes a viral protein, named Mat, with unknown function. The transcript mat is fully spliced and comprises parts of the coding regions of MA and TM. Interestingly, the expression of Mat depends on Rev and the CRM1 pathway. Rev could specifically bind to Mat mRNA to promote its nuclear export. We further identified that the first exon of Mat mRNA, which is located within the Gag-encoding region, acts as an unreported RRE. Altogether, we identified a novel fully spliced transcript mat with an unusual RRE, which interacts with Rev for nuclear export through the CRM1 pathway. Our findings may help to expend the understanding of gene transcription and expression of lentivirus. Author summaryIn lentiviruses, the nuclear export of viral transcripts is an important step in controlling viral gene expression. Generally, the unspliced and incompletely spliced (that is, intron-containing) transcripts are exported via the CRM1-dependent export pathway in a process mediated by the viral Rev protein by binding to the Rev-responsive element (RRE) located within the Env-coding region. However, the completely spliced (intronless) transcripts are exported via an endogenous cellular pathway which is Rev independent. Here we identified a novel intronless transcript from EIAV and demonstrated that it encodes a viral protein, termed Mat. Interestingly, we have determined that the expression of Mat depends on Rev, and identified that the first exon of Mat mRNA could specifically bind to Rev and be exported to the cytoplasm, which suggests that first exon of Mat mRNA is a second RRE of EIAV. These findings update the EIAV genome structure and highlight the diversification of post-transcriptional regulation patterns in EIAV, and provides important insights into the Rev-dependent nuclear export of completely spliced transcripts in lentiviruses.

molecular biology↗

bioRxiv2021

Keap1 recognizes EIAV early accessory protein Rev to promote antiviral defense

The Nrf2/Keap1 axis plays a complex role in viral susceptibility, virus-associated inflammation and immune regulation. However, whether or how the Nrf2/Keap1 axis is involved in the interactions between equine lentiviruses and their hosts remains unclear. Here, we demonstrate that the Nrf2/Keap1 axis was activated during EIAV infection. Mechanistically, EIAV-Rev competitively binds to Keap1 and releases Nrf2 from Keap1-mediated repression, leading to the accumulation of Nrf2 in the nucleus and promoting Nrf2 responsive genes transcription. Subsequently, we demonstrated that the Nrf2/Keap1 axis represses EIAV replication via two independent molecular mechanisms: directly increasing antioxidant enzymes to promote effective cellular resistance against EIAV infection, and repression of Rev-mediated RNA transport through direct interaction between Keap1 and Rev. Together, these data suggest that activation of the Nrf2/Keap1 axis mediates a passive defensive response to combat EIAV infection. The Nrf2/Keap1 axis could be a potential target for developing the strategies for combating EIAV infection. Author summaryHere we report that the Nrf2/Keap1 axis acts as an antiviral effector on EIAV replication through two-way regulation of Rev. On the one hand, EIAV-Rev activates the Nrf2/Keap1 axis by competitive interaction with Keap1, which promotes the transcription of cytoprotective genes implicated in the antiviral response. On the other hand, Keap1 restricts Rev/RRE-dependent RNA transport, leading to inhibition of viral protein synthesis and reduction in viral replication. This study highlights the importance of the Nrf2/Keap1 axis in controlling EIAV replication, and identifies this pathway as a potential new entry-point for treating lentivirus infection. Importantly, this report provides new insights into the regulation of viral replication by the Nrf2/Keap1 axis.

microbiology↗

bioRxiv2020

Regeneration of Functional Retinal Ganglion Cells by Neuronal Identity Reprogramming

Degeneration of retinal ganglion cells (RGCs) and their axons underlies vision loss in glaucoma and various optic neuropathies. There are currently no treatments available to restore lost vision in patients affected by these diseases. Regenerating RGCs and reconnecting the retina to the brain represent an ideal therapeutic strategy; however, mammals do not have a reservoir of retinal stem/progenitor cells poised to produce new neurons in adulthood. Here, we regenerated RGCs in adult mice by direct lineage reprogramming of retinal interneurons. We successfully converted amacrine and displaced amacrine interneurons into RGCs, and observed that regenerated RGCs projected axons into brain retinorecipient areas. They convey visual information to the brain in response to visual stimulation, and are able to transmit electrical signals to postsynaptic neurons, in both normal animals and in a diseased model. The generation of functional RGCs in adult mammals points to a therapeutic strategy for vision restoration in patients.

neuroscience↗

bioRxiv2020

Organogenesis and Vasculature of Anaxagorea Revealing the Axial Homologs in the Carpel and its Implications for the Origin of Angiosperms

Elucidating the origin of carpel has been a challenge in botany for a long time. The Unifying Theory suggested that the carpel originate from a composite organ comprising an ovule-bearing shoot and a foliar part enclosing the shoot. A logical inference from this theory is that placenta in angiosperms should have radiosymmetrical vasculature, just like that in a young branch. Anaxagorea is the most basal genus of the primitive angiosperm family, Annonaceae. The conspicuous carpel stipe makes it an ideal material for exploring the carpel vasculature. In this study, serial sections of flower and carpel were delineated in Anaxagorea luzonensis and A. javanica, and a three-dimensional model of the carpel vasculature was reconstructed. The results show that (1) vascular bundles at both the carpel stipe and the ovule/placenta are in a radiosymmetrical pattern, (2) the amphicribral bundles would develop into ring-arranged bundle complex with the carpel maturation, (3) the ovule/placenta bundles were separated from the bundles of the carpel wall, and, (4) all the radiosymmetrical vasculature (including amphicribral bundles and ring-arranged bundle complexes) in the carpel were fed by a larger radiosymmetrical bundle system. These results suggest that the radiosymmetrical pattern of carpel vasculature are in line with the Unifying Theory.

evolutionary biology↗

bioRxiv2019

BTB-TAZ domain protein MdBT2 modulates malate accumulation by targeting a bHLH transcription factor for degradation in response to nitrate

Excessive application of nitrate, an essential macronutrient and a signal regulating diverse physiological processes, decreases malate accumulation in apple fruit, but the underlying mechanism remains poorly understood. Here, we show that an apple BTB/TAZ protein MdBT2 is involved in regulating malate accumulation and vacuolar pH in response to nitrate. In vitro and in vivo assays indicate that MdBT2 interacts directly with and ubiquitinates a bHLH transcription factor, MdCIbHLH1, via the ubiquitin/26S proteasome pathway in response to nitrate. This ubiquitination results in the degradation of MdCIbHLH1 protein and reduces the transcription of MdCIbHLH1-targeted genes involved in malate accumulation and vacuolar acidification including MdVHA-A encoding a vacuolar H+-ATPase gene, and MdVHP1 encoding a vacuolar H+-pyrophosphatase gene, as well as MdALMT9 encoding a aluminum-activated malate transporter gene. A series of transgenic analyses in apple materials including fruits, plantlets and calli demonstrate that MdBT2 controls nitrate-mediated malate accumulation and vacuolar pH at least partially, if not completely, via regulating the MdCIbHLH1 protein level. Taken together, these findings reveal that MdBT2 regulates the stability of MdCIbHLH1 via ubiquitination in response to nitrate, which in succession transcriptionally reduces the expression of malate-associated genes, thereby controlling malate accumulation and vacuolar acidification in apples under high nitrate supply.

molecular biology↗

bioRxiv2019

Single-cell RNA sequencing of adult Drosophila ovaryidentifies transcriptional programs governing oogenesis

Oogenesis is a complex developmental process that involves spatiotemporally regulated coordination between the germline and supporting, somatic cell populations. This process has been modelled extensively using the Drosophila ovary. While different ovarian cell types have been identified through traditional means, the large-scale expression profiles underlying each cell type remain unknown. Using single-cell RNA sequencing technology, we have built a transcriptomic dataset for the adult Drosophila ovary and connected tissues. This dataset captures the entire transcriptional trajectory of the developing follicle cell population over time. Our findings provide detailed insight into processes such as cell-cycle switching, migration, symmetry breaking, nurse cell engulfment, egg-shell formation, and signaling during corpus luteum formation, marking a newly identified oogenesis-to-ovulation transition. Altogether, these findings provide a broad perspective on oogenesis at a single-cell resolution while revealing new genetic markers and fate-specific transcriptional signatures to facilitate future studies.

developmental biology↗

bioRxiv2019

The Relationship between Parasitic Fleas and Small Mammals in Household of Western Yunnan Province, China

The Yunnan Province has one of the most serious outbreaks of the plague epidemic in China. Small mammals and fleas are risk factors for the occurrence of plague in commensal plague foci. Understanding the relationship between parasitic fleas and small mammals will help control fleas and prevent the onset of the plague. Four hundred and twenty-one small mammals, belonging to 9 species, were captured. Of these, 170 small mammals (40.4%) were infested with fleas. A total of 992 parasitic fleas (including 5 species) was collected. The number of Leptopsylla Segnis and Xenopsylla Cheopis was 91.0%. The final multiple hurdle negative binomial regression model showed that when compared with Rattus Tanezumi, the probability of flea infestation on Mus musculus and other host species decreased from 58% to 99%, while the infestation with fleas from other host species increased 4.7 fold. The probability of flea prevalence in adult hosts increased by 74%, while the number of fleas decreased by 76%. The number of flea infestations in small male mammals increased by 62%. The number of fleas in small mammals weighing more than 59 grams has been multiplied by about 4. Rattus Tanezumi is the predominant species in households in West Yunnan Province, while Leptopsylla Segnis and Xenopsylla Cheopis are dominant parasitic fleas. There is a strong relationship between the abundance of parasitic fleas and the characteristics of small mammals (e.g. Species, age, sex, and body weight).

zoology↗

bioRxiv2017

Nutrition Outweighs Defense: Myzus persicae (Green Peach Aphid) Prefers and Performs Better on Young Leaves of Cabbage

Plant leaves of different ages differ in nutrition and toxic metabolites and thus exhibit various resistance levels against insect herbivores. However, little is known about the relationship between leaf ontogeny and plant resistance against phloem-feeding insects. In this study, we found that the green peach aphid, Myzus persicae Sulzer, preferred to settle on young cabbage leaves (Brassica oleracea L. var. capitata) rather than mature or old leaves, although young leaves contained the highest concentration of glucosinolates. Furthermore, aphids feeding on young leaves had higher levels of glucosinolates in their bodies, but aphids performed better on young leaves in terms of body weight and population growth. The concentration of glutamine in young leaves was the highest, which stimulated aphids feeding when added to the sucrose solution. Phloem sap of young leaves had higher amino acid:sucrose molar ratio than mature leaves, and aphids feeding on young leaves showed two times longer phloem feeding time and five times more dry honeydew excretion than on other leaves. These results indicate that aphids acquired the highest amount of nutrition and defensive metabolites when feeding on young cabbage leaves that are strong natural plant sinks. The higher phloem sap availability of young leaves likely contributes to the attractiveness and suitability for aphids and may compensate the negative effects of glucosinolates on aphids. According to these findings, we propose that phloem sap availability influenced by leaf ontogeny and source-sink status play a significant role in plant-aphid interaction, which desires more attention in future research.

ecology↗