Chromosome-level genome assembly of Bactrocera dorsalis reveals its adaptation and invasion mechanisms

AbstractBactrocera dorsalis is an invasive polyphagous pest causing considerable ecological and economic damage worldwide. We report a high-quality chromosome-level genome assembly and combine various transcriptome data to explore the molecular mechanisms of its rapid adaptation to new environments. The expansions of the DDE transposase superfamily and key gene families related to environmental adaptation and enrichment of the expanded and unique gene families in metabolism and defence response pathways explain its environmental adaptability. The relatively high but not significantly different expression of heat-shock proteins, regardless of the environmental conditions, suggests an intrinsic mechanism underlying its adaptation to high temperatures. The mitogen-activated protein kinase pathway plays a key role in adaptation to new environments. The prevalence of duplicated genes in its genome explains the diversity in the B. dorsalis complex. These findings provide insights into the genetic basis of the invasiveness and diversity of B. dorsalis, explaining its rapid adaptation and expansion.

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Whole-Genome Sequencing and Genome-Wide Studies of Spiny Head Croaker (Collichthys lucidus) Reveals Potential Insights for Well-Developed Otoliths in the Family Sciaenidae

Frontiers in Genetics ◽

10.3389/fgene.2021.730255 ◽

2021 ◽

Vol 12 ◽

Author(s):

Wu Gan ◽

Chenxi Zhao ◽

Xinran Liu ◽

Chao Bian ◽

Qiong Shi ◽

...

Keyword(s):

Genome Assembly ◽

Molecular Mechanisms ◽

Gene Families ◽

Northwestern Pacific ◽

Draft Assembly ◽

Genome Wide ◽

Long Reads ◽

The Family ◽

Collichthys Lucidus ◽

Chromosome Level

Spiny head croaker (Collichthys lucidus), belonging to the family Sciaenidae, is a small economic fish with a main distribution in the coastal waters of Northwestern Pacific. Here, we constructed a nonredundant chromosome-level genome assembly of spiny head croaker and also made genome-wide investigations on genome evolution and gene families related to otolith development. A primary genome assembly of 811.23 Mb, with a contig N50 of 74.92 kb, was generated by a combination of 49.12-Gb Illumina clean reads and 35.24 Gb of PacBio long reads. Contigs of this draft assembly were further anchored into chromosomes by integration with additional 185.33-Gb Hi-C data, resulting in a high-quality chromosome-level genome assembly of 817.24 Mb, with an improved scaffold N50 of 26.58 Mb. Based on our phylogenetic analysis, we observed that C. lucidus is much closer to Larimichthys crocea than Miichthys miiuy. We also predicted that many gene families were significantly expanded (p-value <0.05) in spiny head croaker; among them, some are associated with “calcium signaling pathway” and potential “inner ear functions.” In addition, we identified some otolith-related genes (such as otol1a that encodes Otolin-1a) with critical deletions or mutations, suggesting possible molecular mechanisms for well-developed otoliths in the family Sciaenidae.

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Chromosome-level genome assembly of the sweet potato weevil, Cylas formicarius (Fabricius) (Coleoptera: Brentidae) and functional characteristics of CforOBP4-6

10.22541/au.162460541.11570297/v1 ◽

2021 ◽

Author(s):

Jinfeng Hua ◽

Lei Zhang ◽

Xiaofeng Dong ◽

Yonghua Han ◽

Xiaowan Gou ◽

...

Keyword(s):

Sweet Potato ◽

Genome Assembly ◽

New Technologies ◽

Gene Families ◽

Sequence Length ◽

Economic Damage ◽

Comparative Genomic ◽

High Quality ◽

Cylas Formicarius ◽

Chromosome Level

Cylas formicarius is one of the most important pests of sweet potato worldwide, causing considerable ecological and economic damage. To improve the effect of comprehensive management and understanding of genetic mechanisms, the genetic functions of C. formicarius have been the subject of intensive study. Using Illumina and PacBio sequencing, we obtained a chromosome-level genome assembly of adult weevils from lines inbred for 15 generations. The high-quality assembly obtained had a size of 338.84 Mb, with contig and scaffold N50 values of 14.97 Mb and 34.23 Mb, respectively. In total, 157.51 Mb of repeat sequences and 11,907 protein-coding genes were predicted. A total of 337.06 Mb of genomic sequences was located on the 11 chromosomes, and the sequence length that could be used to determine the sequence and direction accounted for 99.03% of the total length of the associated chromosome. Comparative genomic analysis showed that C. formicarius was sister to Dendroctonus ponderosae, and C. formicarius diverged from D. ponderosae approximately 138.89 million years ago (Mya). Many important gene families that were expanded in the C. formicarius genome were involved in the chemosensory system. In an in-depth study, the binding assay results indicated that CforOBP4-6 had strong binding affinities for sex pheromones and other ligands. Overall, the high-quality C. formicarius genome provides a valuable resource to reveal the molecular ecological basis, genetic mechanism and evolutionary process of major agricultural pests, deepen the understanding of environmental adaptability and apparent plasticity, and provide new ideas and new technologies for ecologically sustainable pest control.

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Amynthas corticis genome reveals molecular mechanisms behind global distribution

Communications Biology ◽

10.1038/s42003-021-01659-4 ◽

2021 ◽

Vol 4 (1) ◽

Author(s):

Xing Wang ◽

Yi Zhang ◽

Yufeng Zhang ◽

Mingming Kang ◽

Yuanbo Li ◽

...

Keyword(s):

Genome Assembly ◽

Molecular Mechanisms ◽

Gene Families ◽

The Body ◽

Gene Family Evolution ◽

Complex Environments ◽

Protein Coding ◽

Itraq Analysis ◽

Rdna Sequencing ◽

Long Read

AbstractEarthworms (Annelida: Crassiclitellata) are widely distributed around the world due to their ancient origination as well as adaptation and invasion after introduction into new habitats over the past few centuries. Herein, we report a 1.2 Gb complete genome assembly of the earthworm Amynthas corticis based on a strategy combining third-generation long-read sequencing and Hi-C mapping. A total of 29,256 protein-coding genes are annotated in this genome. Analysis of resequencing data indicates that this earthworm is a triploid species. Furthermore, gene family evolution analysis shows that comprehensive expansion of gene families in the Amynthas corticis genome has produced more defensive functions compared with other species in Annelida. Quantitative proteomic iTRAQ analysis shows that expression of 147 proteins changed in the body of Amynthas corticis and 16 S rDNA sequencing shows that abundance of 28 microorganisms changed in the gut of Amynthas corticis when the earthworm was incubated with pathogenic Escherichia coli O157:H7. Our genome assembly provides abundant and valuable resources for the earthworm research community, serving as a first step toward uncovering the mysteries of this species, and may provide molecular level indicators of its powerful defensive functions, adaptation to complex environments and invasion ability.

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The TGFβ-induced phosphorylation and activation of p38 mitogen-activated protein kinase is mediated by MAP3K4 and MAP3K10 but not TAK1

Open Biology ◽

10.1098/rsob.130067 ◽

2013 ◽

Vol 3 (6) ◽

pp. 130067 ◽

Cited By ~ 16

Author(s):

Gopal P. Sapkota

Keyword(s):

Protein Kinase ◽

P38 Mapk ◽

Transforming Growth Factor Beta ◽

Molecular Mechanisms ◽

Epithelial To Mesenchymal Transition ◽

Transforming Growth Factor ◽

Mitogen Activated Protein Kinase ◽

Mapk Phosphorylation ◽

Mesenchymal Transition ◽

Mitogen Activated Protein

The signalling pathways downstream of the transforming growth factor beta (TGFβ) family of cytokines play critical roles in all aspects of cellular homeostasis. The phosphorylation and activation of p38 mitogen-activated protein kinase (MAPK) has been implicated in TGFβ-induced epithelial-to-mesenchymal transition and apoptosis. The precise molecular mechanisms by which TGFβ cytokines induce the phosphorylation and activation of p38 MAPK are unclear. In this study, I demonstrate that TGFβ-activated kinase 1 (TAK1/MAP3K7) does not play a role in the TGFβ-induced phosphorylation and activation of p38 MAPK in MEFs and HaCaT keratinocytes. Instead, RNAi -mediated depletion of MAP3K4 and MAP3K10 results in the inhibition of the TGFβ-induced p38 MAPK phosphorylation. Furthermore, the depletion of MAP3K10 from cells homozygously knocked-in with a catalytically inactive mutant of MAP3K4 completely abolishes the TGFβ-induced phosphorylation of p38 MAPK, implying that among MAP3Ks, MAP3K4 and MAP3K10 are sufficient for mediating the TGFβ-induced activation of p38 MAPK.

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Role of Reactive Oxygen Species in Cancer Progression: Molecular Mechanisms and Recent Advancements

Biomolecules ◽

10.3390/biom9110735 ◽

2019 ◽

Vol 9 (11) ◽

pp. 735 ◽

Cited By ~ 79

Author(s):

Vaishali Aggarwal ◽

Hardeep Tuli ◽

Ayşegül Varol ◽

Falak Thakral ◽

Mukerrem Yerer ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Protein Kinase ◽

Cancer Cell ◽

Cancer Progression ◽

Molecular Mechanisms ◽

Reactive Oxygen ◽

Mitogen Activated Protein Kinase ◽

Oxygen Species ◽

Mitogen Activated Protein ◽

High Concentrations

Reactive oxygen species (ROS) play a pivotal role in biological processes and continuous ROS production in normal cells is controlled by the appropriate regulation between the silver lining of low and high ROS concentration mediated effects. Interestingly, ROS also dynamically influences the tumor microenvironment and is known to initiate cancer angiogenesis, metastasis, and survival at different concentrations. At moderate concentration, ROS activates the cancer cell survival signaling cascade involving mitogen-activated protein kinase/extracellular signal-regulated protein kinases 1/2 (MAPK/ERK1/2), p38, c-Jun N-terminal kinase (JNK), and phosphoinositide-3-kinase/ protein kinase B (PI3K/Akt), which in turn activate the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), matrix metalloproteinases (MMPs), and vascular endothelial growth factor (VEGF). At high concentrations, ROS can cause cancer cell apoptosis. Hence, it critically depends upon the ROS levels, to either augment tumorigenesis or lead to apoptosis. The major issue is targeting the dual actions of ROS effectively with respect to the concentration bias, which needs to be monitored carefully to impede tumor angiogenesis and metastasis for ROS to serve as potential therapeutic targets exogenously/endogenously. Overall, additional research is required to comprehend the potential of ROS as an effective anti-tumor modality and therapeutic target for treating malignancies.

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Saccharomyces cerevisiae and Caffeine Implications on the Eukaryotic Cell

Nutrients ◽

10.3390/nu12082440 ◽

2020 ◽

Vol 12 (8) ◽

pp. 2440

Author(s):

Lavinia Liliana Ruta ◽

Ileana Cornelia Farcasanu

Keyword(s):

Saccharomyces Cerevisiae ◽

Protein Kinase ◽

Molecular Mechanisms ◽

Eukaryotic Cell ◽

Pleiotropic Effect ◽

Mitogen Activated Protein Kinase ◽

Active Principle ◽

Cell Integrity ◽

Tor Signaling ◽

Mitogen Activated Protein

Caffeine–a methylxanthine analogue of the purine bases adenine and guanine–is by far the most consumed neuro-stimulant, being the active principle of widely consumed beverages such as coffee, tea, hot chocolate, and cola. While the best-known action of caffeine is to prevent sleepiness by blocking the adenosine receptors, caffeine exerts a pleiotropic effect on cells, which lead to the activation or inhibition of various cell integrity pathways. The aim of this review is to present the main studies set to investigate the effects of caffeine on cells using the model eukaryotic microorganism Saccharomyces cerevisiae, highlighting the caffeine synergy with external cell stressors, such as irradiation or exposure to various chemical hazards, including cigarette smoke or chemical carcinogens. The review also focuses on the importance of caffeine-related yeast phenotypes used to resolve molecular mechanisms involved in cell signaling through conserved pathways, such as target of rapamycin (TOR) signaling, Pkc1-Mpk1 mitogen activated protein kinase (MAPK) cascade, or Ras/cAMP protein kinase A (PKA) pathway.

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Expression and modulation of p42/p44 MAPKs and cell cycle regulatory proteins in rat pancreas regeneration

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1999.277.5.g953 ◽

1999 ◽

Vol 277 (5) ◽

pp. G953-G959 ◽

Cited By ~ 7

Author(s):

Jean Morisset ◽

JoséCristobal Aliaga ◽

Ezéquiel L. Calvo ◽

Judith Bourassa ◽

Nathalie Rivard

Keyword(s):

Cell Cycle ◽

Molecular Mechanisms ◽

Kinase Inhibitors ◽

Regulatory Proteins ◽

Mitogen Activated Protein Kinase ◽

Cyclin Dependent Kinase ◽

Mapk Activation ◽

Pancreas Regeneration ◽

Mitogen Activated Protein ◽

Cell Cycle Regulatory Proteins

Pancreatic growth occurs after CCK, CCK-induced pancreatitis, and pancreatectomy; the mechanisms involved remain unknown. This study evaluates mitogen-activated protein kinase (MAPK) activation and expression of cell cycle regulatory proteins after pancreatectomy to understand the cellular and molecular mechanisms involved in pancreas regeneration. Rats were killed 1–12 days after pancreatectomy, and p42/p44 MAPK activation, expression of the cyclins D and E, cyclin-dependent kinase (Cdk)-2 activity, retinoblastoma protein (pRb) hyperphosphorylation, and expression of the cyclin kinase inhibitors p15, p21, and p27 were examined. Pancreatic remnants exhibited sustained p42/p44 MAPK activation within 8 h. Cyclins D1 and E showed maximal expression after 2 and 6 days, coinciding with maximal hyperphosphorylation of pRb and Cdk2 activity. The expression of p15 vanished after 12 h, p27 disappeared gradually, and p21 increased early. The p27 complexed with Cdk2 dissociated after 2 days, whereas p21 associated in a reverse fashion. In conclusion, sustained activation of p42/p44 MAPKs and Cdk2 along with overexpression of cyclins D1 and E and reduction of p15 and p27 cyclin inhibitors occurred early after pancreatectomy and are active factors involved in signaling that leads to pancreas regeneration.

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Heregulin Induces Transcriptional Activation of the Progesterone Receptor by a Mechanism That Requires Functional ErbB-2 and Mitogen-Activated Protein Kinase Activation in Breast Cancer Cells

Molecular and Cellular Biology ◽

10.1128/mcb.23.3.1095-1111.2003 ◽

2003 ◽

Vol 23 (3) ◽

pp. 1095-1111 ◽

Cited By ~ 62

Author(s):

Leticia Labriola ◽

Mariana Salatino ◽

Cecilia J. Proietti ◽

Adalí Pecci ◽

Omar A. Coso ◽

...

Keyword(s):

Breast Cancer ◽

Progesterone Receptor ◽

Transcriptional Activation ◽

Molecular Mechanisms ◽

Primary Cultures ◽

Mitogen Activated Protein Kinase ◽

Type I ◽

Mobility Shift ◽

T47d Cells ◽

Mitogen Activated Protein

ABSTRACT The present study addresses the capacity of heregulin (HRG), a ligand of type I receptor tyrosine kinases, to transactivate the progesterone receptor (PR). For this purpose, we studied, on the one hand, an experimental model of hormonal carcinogenesis in which the synthetic progestin medroxyprogesterone acetate (MPA) induced mammary adenocarcinomas in female BALB/c mice and, on the other hand, the human breast cancer cell line T47D. HRG was able to exquisitely regulate biochemical attributes of PR in a way that mimicked PR activation by progestins. Thus, HRG treatment of primary cultures of epithelial cells of the progestin-dependent C4HD murine mammary tumor line and of T47D cells induced a decrease of protein levels of PRA and -B isoforms and the downregulation of progesterone-binding sites. HRG also promoted a significant increase in the percentage of PR localized in the nucleus in both cell types. DNA mobility shift assay revealed that HRG was able to induce PR binding to a progesterone response element (PRE) in C4HD and T47D cells. Transient transfections of C4HD and T47D cells with a plasmid containing a PRE upstream of a chloramphenicol acetyltransferase (CAT) gene demonstrated that HRG promoted a significant increase in CAT activity. In order to assess the molecular mechanisms underlying PR transactivation by HRG, we blocked ErbB-2 expression in C4HD and T47D cells by using antisense oligodeoxynucleotides to ErbB-2 mRNA, which resulted in the abolishment of HRG's capacity to induce PR binding to a PRE, as well as CAT activity in the transient-transfection assays. Although the inhibition of HRG binding to ErbB-3 by an anti-ErbB-3 monoclonal antibody suppressed HRG-induced PR activation, the abolishment of HRG binding to ErbB-4 had no effect on HRG activation of PR. To investigate the role of mitogen-activated protein kinases (MAPKs), we used the selective MEK1/MAPK inhibitor PD98059. Blockage of MAPK activation resulted in complete abrogation of HRG's capacity to induce PR binding to a PRE, as well as CAT activity. Finally, we demonstrate here for the first time that HRG-activated MAPK can phosphorylate both human and mouse PR in vitro.

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Molecular Mechanisms of Liver Injury and Hepatocarcinogenesis: Focusing on the Role of Stress-Activated MAPK

Pathology Research International ◽

10.1155/2012/172894 ◽

2012 ◽

Vol 2012 ◽

pp. 1-14 ◽

Cited By ~ 33

Author(s):

Hayato Nakagawa ◽

Shin Maeda

Keyword(s):

Liver Injury ◽

Molecular Mechanisms ◽

Mapk Pathway ◽

Mitogen Activated Protein Kinase ◽

Cellular Effects ◽

Wide Range ◽

Mitogen Activated Protein ◽

Compensatory Proliferation

Hepatocellular carcinoma (HCC) is the third most common cause of cancer mortality. Short-term prognosis of patients with HCC has improved recently due to advances in early diagnosis and treatment, but long-term prognosis is still unsatisfactory. Therefore, obtaining a further understanding of the molecular carcinogenic mechanisms and the unique pathogenic biology of HCC is important. The most characteristic process in hepatocarcinogenesis is underlying chronic liver injury, which leads to repeated cycles of hepatocyte death, inflammation, and compensatory proliferation and subsequently provides a mitogenic and mutagenic environment leading to the development of HCC. Recent in vivo studies have shown that the stress-activated mitogen-activated protein kinase (MAPK) cascade converging on c-Jun NH2-terminal kinase (JNK) and p38 plays a central role in these processes, and it has attracted considerable attention as a therapeutic target. However, JNK and p38 have complex functions and a wide range of cellular effects. In addition, crosstalk with each other and the nuclear factor-kappaB pathway further complicate these functions. A full understanding is essential to bring these observations into clinical settings. In this paper, we discuss the latest findings regarding the mechanisms of liver injury and hepatocarcinogenesis focusing on the role of the stress-activated MAPK pathway.

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MAPK signalling in cardiovascular health and disease: molecular mechanisms and therapeutic targets

Clinical Science ◽

10.1042/cs20070430 ◽

2008 ◽

Vol 115 (7) ◽

pp. 203-218 ◽

Cited By ~ 262

Author(s):

Anthony J. Muslin

Keyword(s):

Molecular Mechanisms ◽

Cardiovascular Health ◽

Mapk Pathway ◽

Science Research ◽

Pharmacological Therapy ◽

Model Systems ◽

Mitogen Activated Protein Kinase ◽

Extracellular Signal ◽

Mitogen Activated Protein

Intracellular MAPK (mitogen-activated protein kinase) signalling cascades probably play an important role in the pathogenesis of cardiac and vascular disease. A substantial amount of basic science research has defined many of the details of MAPK pathway organization and activation, but the role of individual signalling proteins in the pathogenesis of various cardiovascular diseases is still being elucidated. In the present review, the role of the MAPKs ERK (extracellular signal-regulated kinase), JNK (c-Jun N-terminal kinase) and p38 MAPK in cardiac hypertrophy, cardiac remodelling after myocardial infarction, atherosclerosis and vascular restenosis will be examined, with attention paid to genetically modified murine model systems and to the use of pharmacological inhibitors of protein kinases. Despite the complexities of this field of research, attractive targets for pharmacological therapy are emerging.

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