Journal of Genetics最新文献

{"title":"JAG1 overexpression partially rescues muscle function in a zebrafish model of duchenne muscular dystrophy.","authors":"Vishakha Nesari, Suresh Balakrishnan, Upendra Nongthomba","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Duchenne muscular dystrophy (DMD) is a severe genetic disorder characterized by progressive muscle degeneration and loss of function due to the absence of dystrophin. In this study, we utilized a zebrafish model with a dmd gene knockout to explore the therapeutic potential of JAG1 overexpression in mitigating DMD-associated muscle dysfunction. Dystrophic zebrafish larvae displayed significant impairments in muscle function, evidenced by reduced swimming abilities, decreased birefringence, and disrupted β-dystroglycan localization, indicative of structural degeneration. Overexpression of JAG1, achieved via plasmid injection, partially restored muscle function, as reflected by improvements in stride length and total swimming distance. However, the structural integrity of slow oxidative muscle fibers remained largely unaffected, with a functional decline from 4 to 8 days post-fertilization (dpf) being more indicative of disease progression than structural changes. These findings suggest that the rescue effect of JAG1 overexpression may not be due to the preservation of slow oxidative fibers but rather through a mechanism that reduces susceptibility to contraction-induced injury. Notably, our study faced limitations related to the control of JAG1 expression levels and tissue specificity. Our results highlight the complexity of DMD pathology, where muscle structure and function do not always correlate, emphasizing the need for refined functional assays to better assess therapeutic outcomes. By incorporating functional recovery assessments at 8-10 dpf, zebrafish models can serve as more predictive preclinical tools, potentially enhancing the translational relevance of findings and reducing risks for patients in clinical trials. This study investigates how increasing the levels of a protein called JAG1 can help improve muscle function in a zebrafish model of DMD. By showing partial recovery of muscle activity, the findings suggest new therapeutic strategies that could potentially slow disease progression and improve patient outcomes.</p>","PeriodicalId":15907,"journal":{"name":"Journal of Genetics","volume":"104 ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of whole-exome data of nonobese NAFLD patients from India reveals association with new markers on functionally relevant genes and pathways.","authors":"Arnab Ghosh, Anamita Barik, Rajesh K Rai, Jeffrey D Wall, Abhijit Chowdhury, Parha P Majumder","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Nonalcoholic fatty liver disease (NAFLD) occurs in a significant number of nonobese individuals, especially in Asian populations. Many genetic loci are associated with NAFLD. However, no exome-wide analysis of polymorphism data to identify asso- ciations with NAFLD is available for nonobese individuals from Asia. We have sought to fill this gap. With informed consent, we selected individuals from a defined population in India and assessed their liver fat-graded per international recommendations, and their demo- graphic and anthropometric data were collected. A set of 153 individuals were identified with high-grade liver fat. For each of these fatty- liver individuals (cases), two controls of the same sex with no or little liver fat were selected, the age and BMI of each control not exceeding 5 years and 5 kg/m², respectively, of the case. Whole-genome sequencing was done for each individual. For association analysis, we selected only nonsynonymous germline single-nucleotide polymorphisms (SNPs) in coding regions located on genes expressed in the liver. We removed SNPs and individuals with compromised quality and informativeness. We carried out association analysis in this high-quality data set and validated the results using a novel bootstrap procedure. On the basis of this high-stringency association analysis using exome- wideSNP data on 438 cases and controls, we identified 30 significant SNPs on 24 genes. Of these, 21 SNPs from 17 genes are hitherto unreported. We have determined that most of the significant SNPs are functionally relevant. Pathway analysis revealed that the genes on which these SNPs are located are involved in liver dysfunction.</p>","PeriodicalId":15907,"journal":{"name":"Journal of Genetics","volume":"104 ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deletion of <i>RAI1</i> noncoding exons 1-2 causes Smith-Magenis syndrome.","authors":"Uri Hamiel, Alina Kurolap, Chofit Chai Gadot, Adi Mory, Anat Bar Shira, Hagit Baris Feldman, Daphna Marom","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Smith-Magenis syndrome (SMS) is a complex genetic disorder characterized by developmental delay and a typical behavioral phenotype. Interstitial 17p11.2 deletions, which include the RAI1 gene are detected in >90% of patients, while single nucleotide variants (SNVs) are detected in the rest. The <i>RAI1</i> gene is encoded from exons 3 onwards, while exons 1-2 are noncoding. It is unclear whether genetic variants preceding exon 3 cause SMS. We evaluated a 15-month-old infant for developmental delay and infantile spasms who was found to carry a deletion encompassing exons 1-2 of <i>RAI</i>. To determine whether the deletion of the noncoding exons 1-2 of the <i>RAI1</i> gene is associated with SMS and to elucidate the underlying mechanism of this association. A singleton exome-based gene panel was performed, followed by chromosomal-microarray (CMA) to confirm the results. Real time quantitative PCR (RT-qPCR) analysis was conducted to evaluate <i>RAI1</i> mRNA expression. CMA confirmed a de novo 737.8 kbp deletion on 17p11.2, which includes exons 1-2 of <i>RAI1</i> but spares exons 3 onwards. RT-qPCR analysis on RNA extracted from the patient, father and three unrelated controls revealed that the patient has <i>RAI1</i> haploinsufficiency. We show that deletion of the <i>RAI1</i> noncoding exons 1-2, which spares the gene's coding region, causes <i>RAI1</i> haploinsufficiency by eliminating regulatory elements, including the gene promoter, thus causing SMS and expanding the mutational spectrum of SMS.</p>","PeriodicalId":15907,"journal":{"name":"Journal of Genetics","volume":"104 ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel intron variant in the prolactin gene associated with eggshell weight and thickness with putative alternative splicing patterns in chickens","authors":"Dhafer A. Ali, Nihad Abdul-Lateef Ali, Thamer R. S. Aljubouri, Mohammed Baqur S. Al-Shuhaib","doi":"10.1007/s12041-024-01482-w","DOIUrl":"https://doi.org/10.1007/s12041-024-01482-w","url":null,"abstract":"<p>Raising Iraqi indigenous chickens (IIC) is restricted by their thin and low eggshell weights. Due to the importance of the prolactin (<i>Prl</i>) gene in regulating a wide range of egg production traits, this study assessed the potential genetic polymorphisms associated with <i>Prl</i> that may influence these traits. The polymorphism was examined in three <i>Prl</i> loci of the IIC breed (<i>n</i> = 120) in comparison with the standard Hyline breed (<i>n</i> = 120). The polymorphism of both breeds was associated with eggshell weight and thickness indices for 16 weeks, starting from the 44th to the 59th week. After genotyping three loci within <i>Prl</i> by polymerase chain reaction-single-stranded conformation polymorphism (SSCP) method, only one novel SNP was identified in intron 4, namely 129G &gt; A. The identified intron SNP exerted a significant association with both eggshell thickness and weight indices throughout the investigation period. Birds with GG genotype exhibited higher indices of eggshell thickness and weight than those with the GA and AA genotypes, respectively. The employed <i>in silico</i> tools predicted a remarkable ability for the identified SNP to alter the mRNA splicing pattern, which might be related to altered prolactin activity in birds having an alternative allele A. This study is the first to suggest the significance of this novel intron SNP in assessing eggshell traits in chickens.</p>","PeriodicalId":15907,"journal":{"name":"Journal of Genetics","volume":"86 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142260527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of the contribution of VDR and VDBP/GC genes in the pathogenesis of celiac disease","authors":"Pratibha Banerjee, Harinder Singh, Priyanka Tiwari, Ajit Sood, Vandana Midha, Gursewak Singh, B K Thelma, Sabyasachi Senapati","doi":"10.1007/s12041-024-01480-y","DOIUrl":"https://doi.org/10.1007/s12041-024-01480-y","url":null,"abstract":"<p>Vitamin-D deficiency (VDD) is a global health concern. It is known to play a critical role in the immunomodulation, and thus, its metabolism could be investigated to unravel its contribution in common immune-mediated diseases, e.g., celiac disease (CD). Genotyping of SNPs from vitamin D receptor (<i>VDR</i>) gene, such as rs11568820 (Cdx2) and rs2228570 (Fok1) using allele specific multiplex polymerase chain reaction (ASM-PCR) and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) respectively; and rs7041 and rs4588 of vitamin D binding protein (<i>VDBP/GC</i>) using PCR-RFLP were done in 969 subjects including CD cases (<i>n</i>=506) and controls (<i>n</i>=463). Genotype data for 86 CD and 712 controls for rs11568820 and rs7041 were retrieved from already published Immunochip genotype data. Serum concentration of vitamin-D and vitamin D binding protein (VDBP) were measured for 283 participants (98 CD and 185 controls). rs4588-A allele was identified as protective allele [OR=0.6(0.4–0.7), <i>P</i>&lt;0.0001]. Significantly reduced serum level of vitamin-D was observed in CD patients [median=16.25 ng/mL, IQR (8.94–23.60)] than in controls [median=19.94 ng/mL, IQR (13.91–28.46)] with <i>P</i>=0.001. Notably, rs7041-GG, rs4588-CC, and 1F (GC) haplotype of <i>VDBP</i>/<i>GC</i> showed significant association (<i>P</i>&lt;0.05) with reduced serum vitamin D level. We did not find any significant association with VDBP serum concentration. Significant vitamin D and VDBP level correlations were observed in controls (spearman r = 0.3, <i>P</i>=0.005). The present study highlights the significance of reduced vitamin-D serum level in CD. 1F variant of <i>VDBP</i> and lower vitamin-D levels contribute to CD. No correlation between vitamin-D and VDBP levels suggests that vitamin-D supplementation may improve vitamin-D levels but might not affect VDBP levels in CD subjects.</p>","PeriodicalId":15907,"journal":{"name":"Journal of Genetics","volume":"42 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142196522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel missense variant in PNLDC1 associated with nonobstructive azoospermia","authors":"Mouness Rahimian, Masomeh Askari, Najmeh Salehi, Mojtaba Jaafarinia, Mohsen Forouzanfar, Navid Almadani, Andrea Riccio, Mehdi Totonchi","doi":"10.1007/s12041-024-01478-6","DOIUrl":"https://doi.org/10.1007/s12041-024-01478-6","url":null,"abstract":"<p>The most severe type of male infertility is nonobstructive azoospermia (NOA), where there is no sperm in the ejaculate due to failure of spermatogenesis. The predictable frequency of NOA in the general population is one in 100 men. Genetic studies have recognized dozens of NOA genes. Most NOA aetiologies remain idiopathic. Monogenic mutations can be a reason for a part of idiopathic NOA cases. To address this, we studied the pedigree of a consanguineous family with three NOAs by a family-based exome sequencing. Our goal was to pinpoint the genetic variants responsible for idiopathic NOA to aid future clinical genetic diagnostics and treatment strategies. Bioinformatics analysis followed by Sanger sequencing revealed that NOA patients were homozygous for a rare novel missense variant in <i>PNLDC1</i> (NM_173516:exon9:c.710G&gt;A;p.Gly237Asp). <i>In silico,</i> single-cell RNA sequencing data analysis and protein modelling demonstrated that PNLDC1, Gly237Asp resided in the conserved region of the CAF1 domain which could lead to local instability in the structure and alteration of protein phosphorylation site. We conclude that the novel missense <i>PNLDC1</i> variant may affect meiosis and spermatogenesis, leading to NOA and the genetic cause of this idiopathic NOA family. Our result helps genetic counselling for idiopathic NOA cases and provides the occasion for more efficient diagnosis in the clinical setting.</p>","PeriodicalId":15907,"journal":{"name":"Journal of Genetics","volume":"25 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142196505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-7160 inhibits gastric cancer cell proliferation and metastasis by silencing SIX1","authors":"Meng Meng, Guoxin Guan, Xingming Liu, Wei Sun, Xinye Cui, Saiya Fu, Fuwen Luo","doi":"10.1007/s12041-024-01479-5","DOIUrl":"https://doi.org/10.1007/s12041-024-01479-5","url":null,"abstract":"<p>Upregulation of homeoprotein <i>SIX1</i> in gastric cancer (GC) is related to tumour proliferation and invasion. MicroRNA-7160 (miR-7160) is a homeoprotein <i>SIX1</i>-targeting miRNA that downregulates miR-7160, leading to cancer development. Total gastric cancer samples were collected from six patients, and relative expression levels of <i>SIX1</i> mRNA and miRNAs were analysed by qRT-PCR. To evaluate the regulation of <i>SIX1</i> by miR-7160, pGL3-SIX1-mut, pGL3-SIX1, and miR-7160 mimics transfected into cells using lipofectamine 2000. After transfection, proliferation and apoptosis in cultured cells were assessed using the nuclear TUNEL staining and CCK8 reagent, respectively. We demonstrated that the downregulation of miR-7160 in human gastric cancer cells is related to the upregulation of <i>SIX1</i> mRNA. In gastric cancer cell lines, miR-7160 overexpression could downregulate the expression and inhibit cancer cell proliferation and growth <i>in vitro</i>. However, overexpression of miR-7160 did not increase gastric cancer cell apoptosis. <i>In vitro</i> downregulation of <i>SIX1</i> decreased vimentin, N-cadherin, and other EMT-related gene expression and increased E-cadherin expression. In brief, miR-7160, by targeting <i>SIX1</i>, inhibits gastric cancer proliferation and cell growth <i>in vitro</i>, which provides an idea for introducing a new treatment option for gastric cancer.</p>","PeriodicalId":15907,"journal":{"name":"Journal of Genetics","volume":"42 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142196506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"COQ7 splice site variant causing a spastic paraparesis phenotype in siblings","authors":"Haseena Sait, Manmohan Pandey, Shubha R. Phadke","doi":"10.1007/s12041-024-01477-7","DOIUrl":"https://doi.org/10.1007/s12041-024-01477-7","url":null,"abstract":"<p>The <i>COQ7</i> gene is one of the causative genes for primary COQ10 deficiency-related disorders. OMIM-related phenotypes include severe encephalo-myo-nephrocardiopathy and distal hereditary motor neuronopathy. In the present study, we performed the exome sequencing analysis on the proband of a single family with two siblings affected by hereditary spastic paraparesis (HSP). Segregation analysis was conducted on the affected siblings and parents using the Sanger sequencing. <i>In silico</i> secondary and tertiary pre-mRNA structure analysis and protein modelling were carried out. Exome sequencing identified a homozygous splice site variant in the <i>COQ7</i> gene (NM_016138.5: c.367+5G&gt;A) in the proband. Sanger sequencing confirmed the homozygous status in the affected sibling and heterozygous status in both parents, consistent with autosomal recessive inheritance. <i>In silico</i> secondary and tertiary premRNA structure analysis and protein modelling predicted the deleterious nature of the variant. This case highlights a distinct intermediate phenotype of <i>COQ7</i> related disorders comprising early-onset spastic paraparesis due to a novel splice site variant in the <i>COQ7</i> gene. This expands the spectrum of clinical manifestations associated with <i>COQ7</i> deficiency and underscores the importance of considering <i>COQ7</i> gene mutations in the differential diagnosis of HSP.</p>","PeriodicalId":15907,"journal":{"name":"Journal of Genetics","volume":"153 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141587456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expanding the genetic and phenotypic spectrum of Baker–Gordon syndrome: a new de novo SYT1 variant","authors":"Francisco Javier Cotrina-Vinagre, María Elena Rodríguez-García, Lucía Del Pozo-Filíu, Pilar Quijada-Fraile, Francisco Martínez-Azorín","doi":"10.1007/s12041-024-01476-8","DOIUrl":"https://doi.org/10.1007/s12041-024-01476-8","url":null,"abstract":"<p>We report the case of a Spanish pediatric patient with developmental delay, hypotonia, feeding difficulties, visual problems, and hyperkinetic movements. Whole-exome sequencing uncovered a new heterozygous <i>de novo</i> Synaptotagmin 1 (<i>SYT1</i>) missense variant, NM_005639.3:c.930T&gt;A (p.Asp310Glu), in a female proband. This gene encodes the synaptotagmin-1 (SYT1) protein, which is a component of a protein complex involved in the fusion of synaptic vesicles with the presynaptic membrane. Pathogenic <i>SYT1</i> variants have been associated with Baker–Gordon syndrome (BAGOS), an autosomal dominant neurodevelopmental disorder. Although up to 30 cases have been identified worldwide, to the best of our knowledge, this is the first patient described with mitochondrial respiratory chain deficiencies and rod–cone dysfunction. In conclusion, our data expand both the genetic and phenotypic spectrum associated with <i>SYT1</i> variants.</p>","PeriodicalId":15907,"journal":{"name":"Journal of Genetics","volume":"4 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141546691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Detection of caudal type homeobox 1 (CDX1) gene methylated DNA, as a stool-based diagnostic biomarker in colorectal cancer","authors":"Sarina Almasi, Lida Haghnazari, Seyedeh Ozra Hosseini, Nayebali Rezvani","doi":"10.1007/s12041-024-01473-x","DOIUrl":"https://doi.org/10.1007/s12041-024-01473-x","url":null,"abstract":"<p>Colorectal cancer (CRC) is known to develop due to the accumulation of both genetic and epigenetic alterations, resulting in the conversion of intestinal epithelial cells to malignant adenocarcinoma cells. Caudal type homeobox 1 (<i>CDX1</i>) gene is a homeobox transcription factor and a selective tumour suppressor gene that is an important factor for the development of intestinal cells. This gene plays a role in the differentiation of intestinal epithelial cells, and its expression decreases in a number of cell lines derived from CRC, which suggests that a lack of <i>CDX1</i> expression is a risk factor for the development of colorectal carcinoma. Therefore, the methylated DNA amounts of <i>CDX1</i> gene in stool samples were investigated as a noninvasive method for the detection of CRC. In the present study, the methylation of <i>CDX1</i> gene promoter region was assessed in stool samples of 50 CRC patients and 50 healthy individuals by MethyLight PCR using two primers and a Taq Man probe, which was completely specifically designed for fully methylated DNA of the gene promoter region. The percentage of methylated reference (PMR) of the studied gene in all samples was calculated similarly to previous studies. Statistical analysis was performed using SPSS 16. The PMR medians were 3.25 (95% CI: 0.1–100) and 0.1 (95% CI: 0.07–1) in the stool samples of CRC patients and healthy individuals, respectively. The results showed a significant difference in <i>CDX1</i> gene PMR between stool samples of CRC patients and controls (<i>P</i>-value &lt;0.001). According to the results of this study, it can be argued that measurement of <i>CDX1</i> gene DNA in stool samples using the MethyLight PCR has acceptable sensitivity and specificity, and is adequately potential to be used as a noninvasive complementary method for the diagnosis of CRC, along with colonoscopy as the gold standard to this end. This study is the first report on <i>CDX1</i> methylation in stool samples of CRC patients. Therefore, further research should be carried out with a larger sample size to evaluate its efficacy as a diagnostic biomarker in clinical laboratories.</p>","PeriodicalId":15907,"journal":{"name":"Journal of Genetics","volume":"31 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141511349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}