Enhanced Biosynthesis of d-Allulose from a d-Xylose-Methanol Mixture and Its Self-Inductive Detoxification by Using Antisense RNAs in Escherichia coli.

d-Allulose, a C-3 epimer of d-fructose, has great market potential in food, healthcare, and medicine due to its excellent biochemical and physiological properties. Microbial fermentation for d-allulose production is being developed, which contributes to cost savings and environmental protection. A novel metabolic pathway for the biosynthesis of d-allulose from a d-xylose-methanol mixture has shown potential for industrial application. In this study, an artificial antisense RNA (asRNA) was introduced into engineered Escherichia coli to diminish the flow of pentose phosphate (PP) pathway, while the UDP-glucose-4-epimerase (GalE) was knocked out to prevent the synthesis of byproducts. As a result, the d-allulose yield on d-xylose was increased by 35.1%. Then, we designed a d-xylose-sensitive translation control system to regulate the expression of the formaldehyde detoxification operon (FrmRAB), achieving self-inductive detoxification by cells. Finally, fed-batch fermentation was carried out to improve the productivity of the cell factory. The d-allulose titer reached 98.6 mM, with a yield of 0.615 mM/mM on d-xylose and a productivity of 0.969 mM/h.

N4-acetylcytidine acetylation of neurexin 2 in the spinal dorsal horn regulates hypersensitivity in a rat model of cancer-induced bone pain.

Cancer-induced bone pain (CIBP) significantly impacts the quality of life and survival of patients with advanced cancer. Despite the established role of neurexins in synaptic structure and function, their involvement in sensory processing during injury has not been extensively studied. In this study using a rat model of CIBP, we observed increased neurexin 2 expression in spinal cord neurons. Knockdown of neurexin 2 in the spinal cord reversed CIBP-related behaviors, sensitization of spinal c-Fos neurons, and pain-related negative emotional behaviors. Additionally, increased acetylation of neurexin 2 mRNA was identified in the spinal dorsal horn of CIBP rats. Decreasing the expression of N-acetyltransferase 10 (NAT10) reduced neurexin 2 mRNA acetylation and neurexin 2 expression. In PC12 cells, we confirmed that neurexin 2 mRNA acetylation enhanced its stability, and neurexin 2 expression was regulated by NAT10. Finally, we discovered that the NAT10/ac4C-neurexin 2 axis modulated neuronal synaptogenesis. This study demonstrated that the NAT10/ac4C-mediated posttranscriptional modulation of neurexin 2 expression led to the remodeling of spinal synapses and the development of conscious hypersensitivity in CIBP rats. Therefore, targeting the epigenetic modification of neurexin 2 mRNA ac4C may offer a new therapeutic approach for the treatment of nociceptive hypersensitivity in CIBP.

Genome assembly of autotetraploid Actinidia arguta highlights adaptive evolution and enables dissection of important economic traits.

Actinidia arguta, the most widely distributed Actinidia species and the second cultivated species in the genus, can be distinguished from the currently cultivated Actinidia chinensis on the basis of its small and smooth fruit, rapid softening, and excellent cold tolerance. Adaptive evolution of tetraploid Actinidia species and the genetic basis of their important agronomic traits are still unclear. Here, we generated a chromosome-scale genome assembly of an autotetraploid male A. arguta accession. The genome assembly was 2.77 Gb in length with a contig N50 of 9.97 Mb and was anchored onto 116 pseudo-chromosomes. Resequencing and clustering of 101 geographically representative accessions showed that they could be divided into two geographic groups, Southern and Northern, which first diverged 12.9 million years ago. A. arguta underwent two prominent expansions and one demographic bottleneck from the mid-Pleistocene climate transition to the late Pleistocene. Population genomics studies using paleoclimate data enabled us to discern the evolution of the species' adaptation to different historical environments. Three genes (AaCEL1, AaPME1, and AaDOF1) related to flesh softening were identified by multi-omics analysis, and their ability to accelerate flesh softening was verified through transient expression assays. A set of genes that characteristically regulate sexual dimorphism located on the sex chromosome (Chr3) or autosomal chromosomes showed biased expression during stamen or carpel development. This chromosome-level assembly of the autotetraploid A. arguta genome and the genes related to important agronomic traits will facilitate future functional genomics research and improvement of A. arguta.

Transporter mining and metabolic engineering of Escherichia coli for high-level D-allulose production from D-fructose by thermo-swing fermentation.

D-Allulose is an ultra-low-calorie sweetener with broad market prospects in the fields of food, beverage, health care, and medicine. The fermentative synthesis of D-allulose is still under development and considered as an ideal route to replace enzymatic approaches for large-scale production of D-allulose in the future. Generally, D-allulose is synthesized from D-fructose through Izumoring epimerization. This biological reaction is reversible, and a high temperature is beneficial to the conversion of D-fructose. Mild cell growth conditions seriously limit the efficiency of producing D-allulose through fermentation. FryABC permease was identified to be responsible for the transport of D-allulose in Escherichia coli by comparative transcriptomic analysis. A cell factory was then developed by expression of ptsG-F, dpe, and deletion of fryA, fruA, manXYZ, mak, and galE. The results show that the newly engineered E. coli was able to produce 32.33 ± 1.33 g L-1 of D-allulose through a unique thermo-swing fermentation process, with a yield of 0.94 ± 0.01 g g-1 on D-fructose.

Understanding the initiation, delivery and processing of bone cancer pain from the peripheral to the central nervous system.

Bone cancer pain is a complex condition characterized by persistent, sudden, spontaneous pain accompanied by hyperalgesia that typically arises from bone metastases or primary bone tumors, causing severe discomfort and significantly diminishing cancer patients' quality of life and confidence in their ability to overcome the disease. It is widely known that peripheral nerves are responsible for detecting harmful stimuli, which are then transmitted to the brain via the spinal cord, resulting in the perception of pain. In the case of bone cancer, tumors and stromal cells within the bone marrow release various chemical signals, including inflammatory factors, colony-stimulating factors, chemokines, and hydrogen ions. Consequently, the nociceptors located at the nerve endings within the bone marrow sense these chemical signals, generating electrical signals that are then transmitted to the brain through the spinal cord. Subsequently, the brain processes these electrical signals in a complex manner to create the sensation of bone cancer pain. Numerous studies have investigated the transmission of bone cancer pain from the periphery to the spinal cord. However, the processing of pain information induced by bone cancer within the brain remains unclear. With the continuous advancements in brain science and technology, the brain mechanism of bone cancer pain would become more clearly understood. Herein, we focus on summarizing the peripheral nerve perception of the spinal cord transmission of bone cancer pain and provide a brief overview of the ongoing research regarding the brain mechanisms involved in bone cancer pain.

Epitranscriptomic profiling of N4-acetylcytidine-related RNA acetylation in the spinal dorsal horn of rat with cancer-induced bone pain.

Recently, epigenetics involved in the regulation of gene expression has become a research hotspot. This study evaluated N4-acetylcytidine (ac4c) RNA acetylation in the spinal dorsal horn (SDH) of rats with cancer-induced bone pain (CIBP). The ac4C-specific RIP sequencing and NAT10-specific RIP sequencing were performed to identify the differences in ac4C acetylation and gene expression in the SDH between CIBP and sham groups, the relationship with the acetylation-modifying enzyme NAT10, and association analysis was performed. By interfering with the NAT10 expression, the relationship between some up-regulated genes and ac4C acetylation in CIBP was verified. In this study, we demonstrated that bone cancer increases the levels of NAT10 and the overall acetylation, inducing differential ac4C patterns in the SDH of rats. Through verification experiments, it was found that ac4C acetylation of some genes is regulated by NAT10, and differential ac4C patterns in RNA determine the expression of this RNA. We exposed that some CIBP-related gene expression was altered in the SDH of rats, which was regulated by differentially expressed ac4C acetylation.

Methanol-Dependent Carbon Fixation for Irreversible Synthesis of d-Allulose from d-Xylose by Engineered Escherichia coli.

d-Allulose is a rare hexose with great application potential, owing to its moderate sweetness, low energy, and unique physiological functions. The current strategies for d-allulose production, whether industrialized or under development, utilize six-carbon sugars such as d-glucose or d-fructose as a substrate and are usually based on the principle of reversible Izumoring epimerization. In this work, we designed a novel route that coupled the pathways of methanol reduction, pentose phosphate (PP), ribulose monophosphate (RuMP), and allulose monophosphate (AuMP) for Escherichia coli to irreversibly synthesize d-allulose from d-xylose and methanol. After improving the expression of AlsE by SUMO fusion and regulating the carbon fluxes by knockout of FrmRAB, RpiA, PfkA, and PfkB, the titer of d-allulose in fed-batch fermentation reached ≈70.7 mM, with a yield of ≈0.471 mM/mM on d-xylose or ≈0.512 mM/mM on methanol.

Metabolically Engineered Escherichia coli for Conversion of D-Fructose to D-Allulose via Phosphorylation-Dephosphorylation.

D-Allulose is an ultra-low calorie sweetener with broad market prospects. As an alternative to Izumoring, phosphorylation-dephosphorylation is a promising method for D-allulose synthesis due to its high conversion of substrate, which has been preliminarily attempted in enzymatic systems. However, in vitro phosphorylation-dephosphorylation requires polyphosphate as a phosphate donor and cannot completely deplete the substrate, which may limit its application in industry. Here, we designed and constructed a metabolic pathway in Escherichia coli for producing D-allulose from D-fructose via in vivo phosphorylation-dephosphorylation. PtsG-F and Mak were used to replace the fructose phosphotransferase systems (PTS) for uptake and phosphorylation of D-fructose to fructose-6-phosphate, which was then converted to D-allulose by AlsE and A6PP. The D-allulose titer reached 0.35 g/L and the yield was 0.16 g/g. Further block of the carbon flux into the Embden-Meyerhof-Parnas (EMP) pathway and introduction of an ATP regeneration system obviously improved fermentation performance, increasing the titer and yield of D-allulose to 1.23 g/L and 0.68 g/g, respectively. The E. coli cell factory cultured in M9 medium with glycerol as a carbon source achieved a D-allulose titer of ≈1.59 g/L and a yield of ≈0.72 g/g on D-fructose.

Aligned electrospun poly(L-lactide) nanofibers facilitate wound healing by inhibiting macrophage M1 polarization via the JAK-STAT and NF-κB pathways.

Delayed wound healing remains a challenge, and macrophages play an important role in the inflammatory process of wound healing. Morphological changes in macrophages can affect their phenotype, but little is known about the underlying mechanism. Aligned electrospun nanofibers have natural advantages in modulating cell morphology. Therefore, the current study constructed aligned electrospun nanofibers that could transform macrophages into elongated shapes. Our results demonstrated that aligned nanofibers without exogenous cytokines could downregulate the proinflammatory M1 phenotype and upregulate the prohealing M2 phenotype in an inflammatory environment. Importantly, our study revealed that aligned electrospun nanofibers could inhibit macrophage M1 polarization via the JAK-STAT and NF-κB pathways. Furthermore, the conditioned medium from macrophages cultured on aligned nanofibers could encourage fibroblast migration, proliferation and collagen secretion. In vivo, aligned nanofibers alleviated the inflammatory microenvironment, promoted angiogenesis and accelerated wound healing in mouse skin defects by modulating macrophage phenotypes. Collectively, aligned electrospun nanofibers can influence macrophage polarization via the JAK-STAT and NF-κB pathways and attenuate the local inflammatory response in skin wounds. This study provides a potential strategy to modulate macrophage polarization and promote wound healing by controlling the topology of biomaterials and offers a new perspective for the application of nanotechnology in wound healing.

Cobratoxin Alleviates Cancer-Induced Bone Pain in Rats via Inhibiting CaMKII Signaling Pathway after Acting on M4 Muscarinic Cholinergic Receptors.

Cancer-induced bone pain (CIBP) is a common pain in clinics, which can reduce the quality of life and increase the mortality of patients, but the treatment of CIBP is limited. This study was designed to investigate the analgesic effect of α-cobratoxin on CIBP and further to explore the molecular target and potential signal pathway. As shown by the mechanical allodynia test in a CIBP rat model, administration of α-cobratoxin produced significant analgesia in a dose-dependent manner, and the analgesic effects were blocked by pretreatment with an intrathecal injection of M4 mAChR-siRNA or intraperitoneal injection of tropicamide, an antagonist of M4 muscarinic cholinergic receptor. Whole-cell patch-clamp recording showed that α-cobratoxin can decrease the spontaneous firing and spontaneous excitatory postsynaptic currents of SDH neurons in CIBP rats. In primary lumber SDH neurons, intracellular calcium measurement revealed that α-cobratoxin decreased intracellular calcium concentration, and immunofluorescence demonstrated that M4 muscarinic cholinergic receptor and CaMKII/CREB were co-expressed. In the CIBP model and primary SDH neurons, Western blot showed that the levels of p-CaMKII and p-CREB were increased by α-cobratoxin and the effect of α-cobratoxin was antagonized by M4 mAChR-siRNA. The quantitative polymerase chain reaction (qPCR) results showed that α-cobratoxin downregulated the expression of proinflammatory cytokines through M4 muscarinic cholinergic receptor in SDH. These results suggest that α-cobratoxin may activate M4 muscarinic cholinergic receptor, triggering the inhibition of SDH neuronal excitability via CaMKII signaling pathway, thereby resulting in antagonistic effects in the CIBP rat model.

Potential mechanism and key genes involved in mechanical ventilation and lipopolysaccharide­induced acute lung injury.

Mechanical ventilation (MV) and lipopolysaccharide (LPS) infection are common causes of acute lung injury. The aim of the present study was to identify the key genes and potential mechanisms involved in mechanical ventilation (MV) and lipopolysaccharide (LPS)­induced acute lung injury (ALI). Gene expression data of adult C57BL/6 mice with ALI induced by inhaling LPS, MV and LPS + MV were downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) associated with MV, LPS and LPS + MV were screened, followed by functional enrichment analysis, protein­protein interaction network construction, and prediction of transcription factors and small molecule drugs. Finally, the expression of key genes was verified in vivo using reverse transcription­quantitative PCR. A total of 63, 538 and 1,635 DEGs were associated with MV, LPS and LPS + MV, respectively. MV­associated genes were significantly enriched in the 'purine ribonucleotide metabolic process'. LPS and LPS + MV­associated genes were significantly enriched in 'cellular response to cytokine stimulus' and 'cell chemotaxis'. All three conditions were enriched in 'TNF signaling pathway' and 'IL­17 signaling pathway'. Expression levels of C­X­C motif chemokine ligand (CXCL)2, CXCL3 and CXCL10 were upregulated in the LPS and LPS + MV groups. Adenosine A2b receptor, zinc finger and BTB domain­containing 16 and hydroxycarboxylic acid receptor 2 were identified as DEGs in the MV group. Compared with the control group, Early growth response 1 and activating TF 3 was upregulated in all three groups. Similarities and differences were observed among the MV­ and LPS­induced ALI, and MV may enhance the effects of LPS on gene expression. MV may affect urine ribonucleotide metabolic­related processes, whereas LPS may cause cell chemotaxis and cytokine stimulus responses in ALI progression. The inflammatory response was shared by MV and LPS. The results of the present study may provide insight into a theoretical basis for the study and treatment of ALI.

Microfiber-Reinforced Composite Hydrogels Loaded with Rat Adipose-Derived Stem Cells and BMP-2 for the Treatment of Medication-Related Osteonecrosis of the Jaw in a Rat Model.

Severe adverse reactions of bisphosphonates and anti-resorptive or anti-angiogenic medications, termed medication-related osteonecrosis of the jaw (MRONJ), have been reported. MRONJ are difficult to completely cure and could cause great pain to patients. Recent studies have shown that mesenchymal stem cell (MSC) therapies are effective for treating MRONJ, but the method of intravenous injection is unstable and increases the risk of producing tumors. In the present study, low-acyl gellan gum (LAGG) hydrogels were modified with hemicellulose polysaccharide microfibers (PMs) to improve the performance of supporting three-dimensional (3D) cell growth. LAGG-PM composite hydrogels were found to be nontoxic to rat adipose-derived stem cells (rADSCs) in vitro. The hydrogels also promoted the secretion of angiogenic factors, induced osteoclastogenesis by conditioned medium, and supported osteogenic marker expression after the addition of human bone morphogenetic protein-2 (BMP-2). Due to its injectability, the LAGG-PM composite hydrogel incorporated with rADSCs and BMP-2 could be applied into the MRONJ lesion site, which promoted mucosal recovery, bone tissue reconstruction, and osteoclastogenesis. This study confirms the potential applications of LAGG-PM composite hydrogels as 3D cell culture platforms and delivery vehicles for the treatment of MRONJ in a rat model.

Active Learning From Imbalanced Data: A Solution of Online Weighted Extreme Learning Machine.

It is well known that active learning can simultaneously improve the quality of the classification model and decrease the complexity of training instances. However, several previous studies have indicated that the performance of active learning is easily disrupted by an imbalanced data distribution. Some existing imbalanced active learning approaches also suffer from either low performance or high time consumption. To address these problems, this paper describes an efficient solution based on the extreme learning machine (ELM) classification model, called active online-weighted ELM (AOW-ELM). The main contributions of this paper include: 1) the reasons why active learning can be disrupted by an imbalanced instance distribution and its influencing factors are discussed in detail; 2) the hierarchical clustering technique is adopted to select initially labeled instances in order to avoid the missed cluster effect and cold start phenomenon as much as possible; 3) the weighted ELM (WELM) is selected as the base classifier to guarantee the impartiality of instance selection in the procedure of active learning, and an efficient online updated mode of WELM is deduced in theory; and 4) an early stopping criterion that is similar to but more flexible than the margin exhaustion criterion is presented. The experimental results on 32 binary-class data sets with different imbalance ratios demonstrate that the proposed AOW-ELM algorithm is more effective and efficient than several state-of-the-art active learning algorithms that are specifically designed for the class imbalance scenario.

The extent of liver injury determines hepatocyte fate toward senescence or cancer.

It is well known that induction of hepatocyte senescence could inhibit the development of hepatocellular carcinoma (HCC). Until now, it is still unclear how the degree of liver injury dictates hepatocyte senescence and carcinogenesis. In this study, we investigated whether the severity of injury determines cell fate decisions between hepatocyte senescence and carcinogenesis. After testing of different degrees of liver injury, we found that hepatocyte senescence is strongly induced in the setting of severe acute liver injury. Longer-term, moderate liver injury, on the contrary did not result into hepatocyte senescence, but led to a significant incidence of HCC instead. In addition, carcinogenesis was significantly reduced by the induction of severe acute injury after chronic moderate liver injury. Meanwhile, immune surveillance, especially the activations of macrophages, was activated after re-induction of senescence by severe acute liver injury. We conclude that severe acute liver injury leads to hepatocyte senescence along with activating immune surveillance and a low incidence of HCC, whereas chronic moderate injury allows hepatocytes to proliferate rather than to enter into senescence, and correlates with a high incidence of HCC. This study improves our understanding in hepatocyte cell fate decisions and suggests a potential clinical strategy to induce senescence to treat HCC.

Enhanced osteogenic differentiation and bone regeneration of poly(lactic-co-glycolic acid) by graphene via activation of PI3K/Akt/GSK-3ß/ß-catenin signal circuit.

The reconstruction of bone defects by guiding autologous bone tissue regeneration with artificial biomaterials is a potential strategy in the area of bone tissue engineering. The development of new polymers with good biocompatibility, favorable mechanical properties, and osteoinductivity is of vital importance. Graphene and its derivatives have attracted extensive interests due to the exceptional physiochemical and biological properties of graphene. In this study, poly(lactic-co-glycolic acid) (PLGA) films incorporated by graphene nanoplates were fabricated. The results indicated that the incorporation of proper graphene nanoplates into poly(lactic-co-glycolic acid) film could enhance the adhesion and proliferation of rat bone marrow-derived mesenchymal stem cells (rBMSCs). The augmentation of alkaline phosphatase activity, calcium mineral deposition, and the expression level of osteogenic-related genes of rBMSCs on the composite films were observed. Moreover, the incorporation of graphene might activate the PI3K/Akt/GSK-3ß/ß-catenin signaling pathway, which appeared to be the mechanism behind the osteoinductive properties of graphene. Moreover, the in vivo furcation defect implantation results revealed better guiding bone regeneration properties in the graphene-incorporated group. Thus, we highlight this graphene-incorporated film as a promising platform for the growth and osteogenic differentiation of BMSCs that can achieve application in bone regeneration.

Characterization of the duck plague virus UL35 gene.

OBJECTIVE: Previous study has demonstrated that the duck plague virus (DPV) UL35 gene can be expressed as a recombinant fusion protein, and the prepared antiserum has a high reactivity and specificity against the purified recombinant protein. In the present study, to elucidate the properties and functions of its encoding protein, the UL35 gene product (VP26) was identified by using the prepared rabbit polyclonal antiserum. METHODS: Real-time PCR, Western blot and immunofluorescence analysis were used to determine the transcription and expression kinetics and subcellular localization of DPV VP26 in DPV-infected cells. RESULTS: A protein of approximately 13 kDa that reacted with the antiserum was detected in immunoblot of DPV-infected cellular lysates. Real-time PCR and Western blot analysis of DPV-infected cells showed that VP26 was produced predominantly at the late stage of infection, its production was highly dependent on viral DNA synthesis, and the UL35 gene was regulated as a late viral gene, suggesting that the gene should be categorized as gamma2 class. Additionally, analysis of the association of DPV VP26 with purified virions revealed that VP26 was a component of extracellular mature DPV virions. Subcellular localization demonstrated that VP26 firstly localized in cytoplasm, then it transferred to the nucleus and aggregated in the punctate region of the nucleus in DPV-infected cells. CONCLUSION: Taken together, these results will provide a foundation for further functional analysis of the DPV UL35 gene.

Strategic supporting role of a regional state-level hospital during medical rescue after Wenchuan earthquake.

Shortly after the Wenchuan earthquake, the administrative leaders of West China Hospital accurately defined the role of the hospital during the medical rescue work as the treatment center for seriously wounded people, the support center for local hospitals and clinics in the disaster areas in Sichuan Province, and the logistics support center for medical teams from other provinces. Integrated leadership of management and efficient multidepartment co-ordination and co-operation were emphasized. The hospital was immediately transformed from regular mode into a double-track emergency mode. Scientific allocation and dispatch of resources were ensured to meet the changing demand from all levels of rescue work. Three stages were defined based on the conditions of wounded people delivered to the hospital, with different main focuses for each stage. Because of the multidisciplinary co-operation and concerted efforts of a large number of experts from other provinces and countries, an effective and efficient medical rescue service was offered to all wounded people. Until 2 June 2008, 2618 injured people from the disaster area have been treated, of whom 1751 were admitted to the inpatient department, 1135 were seriously wounded, 127 were admitted into the intensive care unit, 1239 underwent surgery, and 77 were treated with haemodialysis. There was an inpatient mortality less than 0.7%. Moreover, even during such a period, routine medical service was offered to patients other than people wounded in the disaster.

Two new flavones from Rubus biflorus Buch.

This project is to study chemical constituents of Rubus biflorus Buch (Chinese name "Fenzhimei"), isolated by silica gel chromatography and structure determined by spectroscopic techniques. Two flavones were isolated from Rubus biflorus Buch and identified as 8-methyl-6-(3"-methylbut-2"-enyl)-5, 7-dihydroxy-5'-methoxy-3', 4'-methylenedioxy flavone (A) and 8-methyl-5-methoxy-6,7-(2", 2"-dimethylpyran)-3', 4'-methylenedioxy-5'-(3'''-methylbut-2'''-enyl) flavone (B), named as fenzhimines A and B, respectively. Compounds A and B are two new flavonoids.

[Cloning of a MADS box protein gene (GhMADS1) from cotton (Gossypium hirsutum L.)].

As a kind of transcription factors, MADS-box protein plays an important role in various cellular processes, especially in the development of floral organs. Based on the contig analysis of the cotton ESTs, the coding region of a cotton MADS-box protein (GhMADS1) was obtained by RT-PCR from floral buds of cotton (G. hirsutum). The cloned fragment of 713 bp (GhMADS1, GenBank accession no. AF538965) contains an open reading frame of 711 bp,coding a polypeptide of 236 amino acids. It was demonstrated that the deduced GhMADS1 protein was highly homologous to the AGL2 group of MADS-box proteins from Vitis vinifera, Nicotiana sylvestris, Petunia hybrida, Arabidopsis thaliana and Antirrhinum majus. Phylogenetic analysis also indicated that GhMADS1 belongs to the AGL2 group of MADS-box proteins. RT-PCR analysis showed that GhMADS1 gene expressed in petals, stamens, ovules and fibers, but not in roots, stems, leaves, bracts and sepals. The strongest expression of GhMADS1 gene was detected in petals. But in floral buds of a cotton homeotic mutant (CHV1), whose floral organs are all converted to bract leaf-like organs, the transcript of GhMADS1 gene was not detected. It was proposed that GhMADS1 gene would be crucial to the development of cotton floral organs.