Biology subjects

Liu, Z.

Publications and source records attributed to Liu, Z..

At least 721 records · Page 40Linked to original sources

bioRxiv2022

Residue-dependent transition temperatures and denaturant midpoints in the folding of a multi-domain protein

As a consequence of the finite size of globular proteins, it is expected that there should be dispersions in the global melting temperature (Tm) and the denaturation midpoint (Cm). Thermodynamic considerations dictate that the dispersions, {Delta}Tm in Tm and {Delta}Cm in Cm, should decrease with N, the number of residues in the protein. We performed coarse-grained simulations of the Self-Organized Polymer (SOP) model of the multi-domain protein, Adenylate Kinase (ADK) with N = 214, in order to calculate thermal and denaturation unfolding titration curves. The results show that [Formula] and [Formula] are non-zero and follow the previously established (Phys. Rev. Lett. 93 268107 (2004)) thermodynamic [Formula] scaling for proteins accurately. For ADK, the dispersions are small ({approx} 0.004), which implies that the melting temperature is more or less unique, which is unlike in BBL (N =40) where [Formula].

biophysics↗

bioRxiv2022

The roles and evolution of the four LEAFY homologues in floral patterning and leaf development in woodland strawberry

The plant-specific transcription factor LEAFY (LFY), generally maintained as a single copy gene in most angiosperm species, plays critical roles in flower and leaf development. However, wild strawberry Fragaria vesca possesses four LFY homologues in the genome, their respective functions and evolution remain unknown. Through chemical mutagenesis screen, we identified two allelic mutations in one of the four LFY homologues, FveLFYa, in F. vesca, causing homeotic conversion of floral organs and reiterative outgrowth of ectopic florets. Both CRISPR-knockout and transgenic rescue confirmed the identity of FveLFYa. Ectopic expression in Arabidopsis lfy-5 mutant revealed that only FveLFYa and FveLFYb can rescue the flower defects and induce solitary flowers in leaf axils. Disruption of FveLFYc, the second abundantly expressed LFY homologue, caused no obvious morphology phenotypes in F. vesca. FveLFYb and FveLFYd are barely expressed. Expression of FveAP1, homologue of the well-known LFY target AtAP1, is not changed in the fvelfya flowers, possibly caused by an absence of any FveLFYa binding site in its promoter. Loss of Axillary Meristems encodes a GRAS transcription factor essential for stamen initiation. The ectopic florets are eliminated in fvelfya lam, suggesting that LAM is required for floret production. Moreover, approximately 30% of mature leaves have smaller or fewer leaflets in fvelfya. Among these homologues, only FveLFYa is syntenic to the homologues in other species. Overall, the detailed analyses of the four LFY homologues in woodland strawberry demonstrate that only FveLFYa plays crucial roles in floral patterning with rewired gene network.

plant biology↗

bioRxiv2022

MeCP2 regulates Gdf11, a dosage-sensitive gene critical for neurological function

Loss- and gain-of-function of MeCP2 causes Rett syndrome (RTT) and MECP2 duplication syndrome (MDS), respectively. MeCP2 binds methyl-cytosines to finely tune gene expression in the brain, though identifying genes robustly regulated by MeCP2 has been difficult. By integrating multiple transcriptomics datasets, we identified that MeCP2 finely regulates Growth differentiation factor 11 (Gdf11). Gdf11 is down-regulated in RTT mouse models and is inversely up-regulated in MDS mouse models. Strikingly, genetically normalizing Gdf11 dosage levels improved several behavioral deficits in a mouse model of MDS. Next, we discovered that losing one copy of Gdf11 alone was sufficient to cause multiple neurobehavioral deficits in mice, most notably hyperactivity and decreased learning and memory. This decrease in learning and memory was not due to changes in proliferation or numbers of progenitor cells in the hippocampus. Lastly, loss of one copy of Gdf11 decreased longevity and survival in mice, corroborating its putative role in aging. Our data demonstrate that Gdf11 dosage is important for brain function.

neuroscience↗

bioRxiv2022

Single-cell chromatin accessibility of developing murine pancreas identifies cell state-specific gene regulatory programs

Numerous studies have characterized the existence of cell subtypes, along with their corresponding transcriptional profiles, within the developing mouse pancreas. The upstream mechanisms that initiate and maintain gene expression programs across cell states, however, remain largely unknown. Here, we generate single-nucleus ATAC-Sequencing data of developing murine pancreas and perform an integrated, multi-omic analysis of both chromatin accessibility and RNA expression to describe the chromatin landscape of both the developing epithelium and mesenchyme at E14.5 at single-cell resolution. We identify candidate transcription factors regulating cell fate and construct gene regulatory networks of active transcription factor binding to regulatory regions of downstream target genes. This work serves as a valuable resource for the field of pancreatic biology in general and contributes to our understanding of lineage plasticity among endocrine cell types. In addition, these data identify which epigenetic states should be represented in the differentiation of stem cells to the pancreatic beta cell fate in order to best recapitulate in vitro the gene regulatory networks that are critical for progression along the beta cell lineage in vivo.

developmental biology↗

bioRxiv2022

Correlation analysis between drug resistance and virulence genes of carbapenem-resistant Acinetobacter baumannii In Western Guilin

BackgoundIn order to detect the resistance of Acinetobacter baumannii to {beta}-lactam antibiotics in western Guilin, analyze the reasons for its resistance, and provide laboratory basis for clinical treatment; method for the {beta}-lactamase gene of Acinetobacter baumannii, and to explore the relationship between the presence of the {beta}-lactamase gene of Acinetobacter baumannii and multidrug resistance. MethodsFrom November 2020 to June 2022, 78 non-repeated Acinetobacter baumannii strains from the Second Affiliated Hospital of Guilin Medical University were collected, and their resistance to carbapenem antibiotics was analyzed. PCR was used to detect resistance-related genes (blaOXA-23, blaOXA-51, blaOXA-58, blaOXA-24, blaIMP and blaSIM) and virulence genes (cusE, abaI and bfmS). To analyze the relationship between drug resistance and virulence genes of Acinetobacter baumannii. ResultsMost of the 165 non-enterobacteriaceae bacteria we collected from the hospital were Acinetobacter baumannii and Pseudomonas aeruginosa, and most of the specimen types were from sputum and secretions, and most of them were from respiratory and critical care diseases area and intensive care unit, among them, there are 78 strains of Acinetobacter baumannii studied this time. After screening, 78 Acinetobacter baumannii strains were resistant to Cefazolin, Ampicillin, Amoxicillin/Clavulanate, Aztreonam, Chloramphenicol, Tetracycline, Cefotaxime, Ampicillin/Sulbactam, Piperacillin, Gentamicin, Ciprofloxacin, Levofloxacin, Moxifloxacin, Cefepime, Ceftazidime, Piperacillin/Tazobactam, Compound Sulfonamide, Meropenem, Imipenem, Amikacin, Polymyxin, resistance rates were 98.72%, 98.72%, 96.16%, 96.15%, 96.15%, 66.67%, 60.26%, 58.98%, 58.97%, 57.69%, 57.69%, 57.69%, 57.69%, 57.69%, 56.41%, 55.13%, 53.85%, 52.56%, 52.56%, 50%, 0%. Among them, 17 strains with drug resistance gene blaOXA-51 were detected,accounting for 21.79%; drug gene blaOXA-23, blaOXA-24, blaIMP, blaOXA-58, blaSIM gene were not detected; 17 strains with virulence gene bfmS was detected, accounting for 21.79%; abaI, csuE virulence gene was not detected. ConclusionAcinetobacter baumannii in the hospital is highly resistant to carbapenems, mainly carrying blaOXA-51 resistance genes. Drug resistance is closely related to the virulence gene bfmS.

microbiology↗

bioRxiv2022

Exosome-derived lncRNA HOXA-AS3 promotes castration resistance and progression of prostate cancer via the miR-29b-3p/Mcl-1/STAT3 axis

Prostate cancer is one of the leading causes of cancer-related deaths in men. While endocrine therapy is effective in the early stage of metastasis, significantly inhibits the progression of metastatic prostate cancer, most patients eventually develop CRPC. Tumor microenvironment are involved in the progression of prostate cancer as an "accomplice", cancer cell-secreted exosomes were identified as crucial messengers can carry lncRNAs to participate in intercellular communication. we revealed PC-3-derived exosomes promote androgen resistance in LNCaP cells. HOXA-AS3 as a ceRNA of miRNA-29b-3p affects the proliferation and invasion ability of prostate cancer cells. A series of molecular experiments, cell experiments and clinical tissue verification experiments confirmed that HOXA-AS3 participates in the castration resistance and progression of prostate cancer through regulating the miR-29b-3p/Mcl-1/STAT3/Cytochrome C/caspases-9 pathway. Dysregulation of HOXA-AS3 is observed in many cancer types, and this study shows the importance of this lncRNA in controlling prostate cancer cell progression, thus highlighting it as a potential biomarker for inhibiting prostate cancer progression and a target for immunotherapy.

genomics↗

bioRxiv2022

Separate roles of LMAN1 and MCFD2 in ER-to-Golgi trafficking of factor V and factor VIII

Mutations in LMAN1 and MCFD2 cause the combined deficiency of FV and FVIII (F5F8D). LMAN1 and MCFD2 form a protein complex that transport FV and FVIII from the endoplasmic reticulum to the Golgi. Although both proteins are required for the cargo receptor function, little is known about specific roles of LMAN1 and MCFD2 in transporting FV/FVIII. We used different LMAN1 and MCFD2 deficient cell lines to investigate the LMAN1/MCFD2-dependent FV/FVIII secretion pathway. LMAN1 deficiency led to more profound decreases in FV/FVIII secretion in HEK293T and HepG2 cells than in HCT116 cells, suggesting regulation of cargo transport by the LMAN1/MCFD2 pathway varies in different cell types. Using these cell lines, we developed functional assays to accurately assess pathogenicity of recently reported potential LMAN1 and MCFD2 missense mutations. LMAN1 with mutations abolishing carbohydrate binding can still partially rescue FV/FVIII secretion, suggesting that N-glycan binding is not absolutely required for FV/FVIII transport. Surprisingly, overexpression of either WT or mutant MCFD2 is sufficient to rescue FV/FVIII secretion defects in LMAN1 deficient cells. These results suggest that cargo binding and transport are carried out by MCFD2 and that LMAN1 primarily serves as a shuttling carrier of MCFD2. Finally, overexpression of both LMAN1 and MCFD2 does not further increase FV/FVIII secretion, suggesting that the amount of the LMAN1-MCFD2 receptor complex is not a rate-limiting factor in ER-Golgi transport of FV/FVIII. This study provides new insight into the molecular mechanism of F5F8D and intracellular trafficking of FV and FVIII. Key PointsO_LIEfficient ER-to-Golgi transport of FV and FVIII requires the LMAN1-MCFD2 cargo receptor complex. C_LIO_LIMCFD2 functions as a primary interacting partner of FV/FVIII cargo and LMAN1 primarily serves as a shuttling carrier of MCFD2. C_LI

cell biology↗

bioRxiv2022

SARS-CoV-2 Omicron boosting induces de novo B cell response in humans

The primary two-dose SARS-CoV-2 mRNA vaccine series are strongly immunogenic in humans, but the emergence of highly infectious variants necessitated additional doses of these vaccines and the development of new variant-derived ones1-4. SARS-CoV-2 booster immunizations in humans primarily recruit pre-existing memory B cells (MBCs)5-9. It remains unclear, however, whether the additional doses induce germinal centre (GC) reactions where reengaged B cells can further mature and whether variant-derived vaccines can elicit responses to novel epitopes specific to such variants. Here, we show that boosting with the original SARS- CoV-2 spike vaccine (mRNA-1273) or a B.1.351/B.1.617.2 (Beta/Delta) bivalent vaccine (mRNA-1273.213) induces robust spike-specific GC B cell responses in humans. The GC response persisted for at least eight weeks, leading to significantly more mutated antigen-specific MBC and bone marrow plasma cell compartments. Interrogation of MBC-derived spike-binding monoclonal antibodies (mAbs) isolated from individuals boosted with either mRNA-1273, mRNA-1273.213, or a monovalent Omicron BA.1-based vaccine (mRNA-1273.529) revealed a striking imprinting effect by the primary vaccination series, with all mAbs (n=769) recognizing the original SARS-CoV-2 spike protein. Nonetheless, using a more targeted approach, we isolated mAbs that recognized the spike protein of the SARS-CoV-2 Omicron (BA.1) but not the original SARS-CoV-2 spike from the mRNA-1273.529 boosted individuals. The latter mAbs were less mutated and recognized novel epitopes within the spike protein, suggesting a naive B cell origin. Thus, SARS-CoV-2 boosting in humans induce robust GC B cell responses, and immunization with an antigenically distant spike can overcome the antigenic imprinting by the primary vaccination series.

immunology↗

bioRxiv2022

Loss of H3.1K27me1 in Arabidopsis confers resistance to Geminivirus by sequestering DNA repair proteins onto rDNA and defense-related genes

The H3 methyltransferases ATXR5 and ATXR6 deposit H3.1K27me1 to heterochromatin to prevent genomic instability and transposon reactivation. Here, we report that atxr5 atxr6 mutants displayed robust resistance to Geminivirus. The viral resistance correlated with activation of DNA repair pathways, but not with transposon reactivation or heterochromatin amplification. We identified RAD51 and RPA1A as partners of virus-encoded Rep protein. The two DNA repair proteins showed increased binding to heterochromatic regions and defense-related genes in atxr5 atxr6 vs wild type plants. Consequently, the proteins had reduced interactions to viral DNA in the mutant, thus hampering viral replication. Additionally, RAD51 recruitment to the host genome arose via BRCA1, HOP2 and CYCB1, and this recruitment was essential for viral resistance in atxr5 atxr6. Thus, Geminiviruses adapt to healthy plants by hijacking its DNA repairing pathways for replication, but the host could retain DNA repairing proteins via sacrificing its genome stability to suppress viral infection.

genetics↗

bioRxiv2022

Literature-based predictions of treatments for genetic disease pathology

Identifying genetic modifiers of disease-causing genes can guide drug discovery for treatment of genetic disorders, but selecting promising drugs to test requires extensive and up-to-date knowledge of drug-gene and gene-gene relationships. To address this challenge, we present PARsing ModifiErS via Abstract aNnotations (PARMESAN), a computational tool that searches PubMed for information on these relationships, and assembles them into one knowledgebase. PARMESAN then hypothesizes on undiscovered drug-gene relationships, assigning an evidence-based score to each hypothesis. We compare PARMESANs drug-gene hypotheses to all of the drug-gene relationships displayed by DrugBank, and see a strong correlation between the prediction score and the predictive accuracy--such that predictions scoring above 10 are 11 times more likely to be correct than incorrect. This publicly available tool provides an automated way to prioritize drug screens to target the most-promising drugs to test, thereby saving time and resources in the development of therapeutics for genetic disorders.

bioinformatics↗

bioRxiv2022

Study on the interactions between cisplatin and cadherin

Cisplatin is an important platinum drug in the chemotherapy of many malignant tumors in clinical application. It is well accepted that its main target is DNA molecule. However, recent studies have shown that platinum drugs may also act on some important functional proteins in the human body and have complicate effects on their efficacy. E-cadherin is newly discovered glycoproteins which have been regarded as the important signs of the occurrence and development of some tumors. In this study, the interactions between cisplatin and E-cadherin were explored by fluorescence spectroscopy and atomic force microscopy (AFM). The fluorescence spectroscopy results indicated that cisplatin can efficiently quench the fluorescence of E-cadherin, and the calculated binding constant Kb was 3.20x106 (25{degrees}C), 1.36 x106(31{degrees}C) and 8.22x105 L mol-1 (37{degrees}C). The thermodynamic parameters {Delta}H <0, {Delta}S <0, {Delta}G <0, reveal that the fluorescence quenching effect of cisplatin on E-cadherin is static quenching, which is dominated by hydrogen bond and van der Waals interaction. The AFM results revealed that there was a staggered interaction between the intermolecular domains of E-cadherin to form a long spherical chain structure. The addition of cisplatin could significantly affect the staggered effect of the E-cadherin molecules. All these results confirmed that there are strong interactions between cisplatin and cadherin.

biochemistry↗

bioRxiv2022

Gene interaction perturbation network deciphers a high-resolution taxonomy in colorectal cancer

Molecular subtypes of colorectal cancer (CRC) are currently identified via the snapshot transcriptional profiles, largely ignoring the dynamic changes of gene expressions. Conversely, biological networks remain relatively stable irrespective of time and condition. Here, we introduce an individual-specific gene interaction perturbation network-based (GIN) approach and identify six GIN subtypes (GINS1-6) with distinguishing features: (i) GINS1 (proliferative, 24%[~]34%), elevated proliferative activity, high tumor purity, immune-desert, PIK3CA mutations, and immunotherapeutic resistance; (ii) GINS2 (stromal-rich, 14%[~]22%), abundant fibroblasts, immune-suppressed, stem-cell-like, SMAD4 mutations, unfavorable prognosis, high potential of recurrence and metastasis, immunotherapeutic resistance, and sensitive to fluorouracil-based chemotherapy; (iii) GINS3 (KRAS-inactivated, 13%[~]20%), high tumor purity, immune-desert, activation of EGFR and ephrin receptors, chromosomal instability (CIN), fewer KRAS mutations, SMOC1 methylation, immunotherapeutic resistance, and sensitive to cetuximab and bevacizumab; (iv) GINS4 (mixed, 10%[~]19%), moderate level of stromal and immune activities, transit-amplifying-like, and TMEM106A methylation; (v) GINS5 (immune-activated, 12%[~]24%), stronger immune activation, plentiful tumor mutation and neoantigen burden, microsatellite instability and high CpG island methylator phenotype, BRAF mutations, favorable prognosis, and sensitive to immunotherapy and PARP inhibitors; (vi) GINS6, (metabolic, 5%[~]8%), accumulated fatty acids, enterocyte-like, and BMP activity. Overall, the novel high-resolution taxonomy derived from an interactome perspective could facilitate more effective management of CRC patients.

genetics↗

bioRxiv2022

The injury-induced circular RNA circGLIS3 activates dermal fibroblasts to promote wound healing

Delayed skin wound healing and excessive scarring are consequences of an impaired healing process and represent a major health and economic burden worldwide. Current intervention strategies lack efficacy and suffer from high recurrence rates necessitating the investigation into alternative treatment modalities like circular RNAs (circRNAs). By RNA sequencing, we profiled circRNA expression changes during human skin wound healing as well as in keratinocytes and fibroblasts isolated from donor-matched skin and acute wounds. CircGLIS3 was found to be transiently upregulated in the dermal fibroblasts upon skin injury, which was at least partially due to the activated IL-1 signaling. Similarly, overabundant circGLIS3 expression was detected in human keloid lesions compared to the surrounding healthy skin. We found that circGLIS3 resided mainly in the cytoplasm, where it interacted with and stabilized Procollagen C-endopeptidase enhancer 1 (PCPE-1) protein to enhance TGF-{beta} signaling, fibroblast activation, and production of extracellular matrix - important biological processes required for wound repair. Accordingly, knockdown of circGLIS3 in human ex vivo wounds potently reduced wound contraction and delayed re-epithelialization. Collectively, we have identified a previously uncharacterized circRNA regulator of human skin wound healing that may open an avenue for circRNA-based therapeutics for abnormal scarring or nonhealing wounds. One Sentence SummaryTransient increase of the circular RNA circGLIS3 promotes the wound fibroblast activation and extracellular matrix production to facilitate wound closure.

molecular biology↗

bioRxiv2022

Detecting rapid pan-cortical voltage dynamics in vivo with a brighter and faster voltage indicator

Widefield imaging with genetically encoded voltage indicators (GEVIs) is a promising approach for understanding the role of large cortical networks in the neural coding of behavior. However, the slow kinetics of current GEVIs limit their deployment for single-trial imaging of rapid neuronal voltage dynamics. Here, we developed a high-throughput platform to screen for GEVIs that combine fast kinetics with high brightness, sensitivity, and photostability under widefield one-photon illumination. Rounds of directed evolution produced JEDI-1P, a green-emitting fluorescent indicator whose performance is improved for all metrics. Next, we optimized a neonatal intracerebroventricular delivery method to achieve cost-effective and wide-spread JEDI-1P expression in mice. We also developed an approach to effectively correct optical measurements from hemodynamic and motion artifacts. Finally, we achieved stable brain-wide voltage imaging and successfully tracked gamma-frequency whisker and visual stimulations in awake mice in single trials, opening the door to investigating the role of high-frequency signals in brain computations.

neuroscience↗

bioRxiv2022

Role of mPFC DUSP1 in regulating the sensitivity to cocaine in adolescent cocaine-exposed mice of adulthood

Adolescent cocaine abuse increases the risk for developing addiction in later life, which remains a big public health concern, but the underlying molecular mechanism is poorly understood. Here, adolescent cocaine-exposed (ACE) male mice models were established by administrating cocaine during adolescent period. When growing to adult age, mice were subjected to conditioned place preference (CPP) to evaluate the sensitivity to cocaine, then potential molecule of dual specificity phosphatase 1 (DUSP1) were screened out by transcriptomic sequencing. Subthreshold dose of cocaine (sdC), that is insufficient to produce CPP, was used to induce CPP in adulthood. The sdC treatment effectively induced CPP in ACE mice during adulthood, accompanied with the more triggered CaMKII-positive neurons, and induced higher Dusp1 gene, lower DUSP1 protein, lower DUSP1 activity and lower DUSP1 expression on CaMKII-positive neurons (DUSP1CaMKII) in medial prefrontal cortex (mPFC). Overexpressing DUSP1CaMKII suppressed CaMKII-positive neuronal activation, and ultimately blocked sdC-induced CPP in ACE mice during adulthood. While, knocking-down DUSP1CaMKII activated more CaMKII-positive neurons, and aggravated sdC-preferred behavior in ACE mice during adulthood. ERK1/2 might be potential subsequent signal for DUSP1 in the process. Collectively, our findings reveal a novel molecular mechanism underlying adolescent drug abuse-induced susceptibility to addiction during adulthood, and mPFC DUSP1CaMKII is a promising pharmacological target to predict or treat addiction, especially caused by adolescent substance use. SummaryAdolescent cocaine exposure causes higher cocaine-preferred behaviors during adulthood, along with evoked mPFC activity in response to cocaine challenge. Locally overexpressing but not knocking-down the dual specificity phosphatase 1 (DUSP1) on CaMKII-positive neurons (DUSP1CaMKII) suppresses mPFC activation, and ultimately rescues the higher sensitivity to cocaine during adulthood.

neuroscience↗

bioRxiv2022

Dynamics of bacterial recombination in the human gut microbiome

Horizontal gene transfer is a ubiquitous force in microbial evolution. Previous studies have shown that the human gut is a hot spot for gene transfer between species, but the more subtle exchange of variation within species - collectively known as recombination - remains poorly characterized in this ecosystem. Here, we show how the genetic structure of the human gut microbiome provides a unique opportunity to measure individual recombination events from sequenced fecal samples, enabling quantitative comparisons of recombination across a diverse range of species that inhabit a common environment. By analyzing a large collection of recent recombination events in the core genomes of 29 gut commensals, we uncovered systematic heterogeneities in the rates and lengths of transferred segments, which are difficult to explain by existing models of ecological isolation or homology-dependent recombination rates. We also find that natural selection plays a role in facilitating the spread of genetic variants onto different strain backgrounds, both within individual hosts and across the broader global population. These results shed light on the dynamics of in situ recombination, which place important constraints on the adaptability of gut microbial communities.

evolutionary biology↗

bioRxiv2022

Cross-amplified Barcodes on Slides for Spatial Transcriptomics Sequencing

Spatial transcriptomics can reveal molecular signatures of tissue at spatial scales, but current technologies cannot integrate excellent accessibility and easy data-decoding. Here, we use oligonucleotides whose number is the square root of the number of spots to generate cross-amplified spatial barcodes on slides using microfluidic technology. This method can obtain microarrays with well-defined barcodes easily and at low cost, without post-decoding, which contributes to the popularization of spatial transcriptomics.

genomics↗

bioRxiv2022

The genome of a vestimentiferan tubeworm (Ridgeia piscesae) provides insights into its adaptation to a deep-sea environment

Vestimentifera (Polychaeta, Siboglinidae) is a taxon of deep-sea worm-like animals living in the deep-sea hydrothermal vent and cold seep areas. The morphology and lifespan of Ridgeia piscesae, which is the only vestimentiferan tubeworm species found in the hydrothermal vents on the Juan de Fuca Ridge, vary greatly according to the endemic environments. Recent analyses have revealed the genomic basis of adaptation in three vent- and seep-dwelling vestimentiferan tubeworms. However, the evolutionary history and mechanism of adaptation in R. piscesae, a unique species in the family Siboglinidae, is remained to be investigated. Here we report a high-quality genome of R. piscesae collected at Cathedral vent of the Juan de Fuca Ridge. Comparative genomic analysis revealed that that the high growth rates of vent-dwelling tubeworms might derive from small genome size. The small genome sizes of these tubeworms are attributed to the repeat content but not the number of genes and intron sizes. Additionally, four genes involved in cell proliferation were subject to positive selection in the genome of R. piscesae, suggesting that, besides apoptosis, cell proliferation is important for regulating growth rate in this species.

genomics↗