Biology subjects

Zhou, L.

Publications and source records attributed to Zhou, L..

At least 325 records · Page 18Linked to original sources

bioRxiv2019

Geographic Patterns of Bacterioplankton among Lakes of the Middle and Lower Reaches of the Yangtze River Basin, China

In aquatic ecosystems, microbial biogeography research is critical for unveiling the mechanisms of microbial community succession. However, little is known about the microbial biogeography among interconnected lakes. To address this deficit, we used high-throughput sequencing to explore geographic patterns and the relative importance of ecological processes that shape these patterns in abundant and rare bacterial subcommunities from 25 lakes across the middle and lower reaches of Yangtze River basin (MLYB, located in southeast China), where most of the lakes are interconnected by river networks. We found that there were significant differences in both abundant and rare bacterial subcommunities between the two lake groups that were far from each other, while were no difference among the nearby lakes in each group. Both abundant and rare bacteria followed a strong distance-decay relationship, especially for rare bacteria. These findings suggest that although the interconnectivity between lakes breaks the geographical isolation of bacteria, the dispersal capability of bacterial taxa was still limited by geographic distance. We also found that although deterministic processes and stochastic processes together drive the bacterial subcommunities assembly, the stochastic processes (based on adjusted R2 in redundancy analysis) exhibited a greater influence on bacterial subcommunities. Our results implied that bacterial dispersal among interconnected lakes was more stochastically. ImportanceUnraveling the relative importance of ecological processes regulating microbial community structure is a central goal in microbial ecology. In aquatic ecosystems, microbial communities often occur in spatially structured habitats, where connectivity directly affects dispersal and metacommunity processes. Recent theoretical work suggests that directional dispersal among connected habitats leads to higher variability in local diversity and among-community composition. However, the study of microbial biogeography among natural interconnected habitats is still lacking. The findings of this study revealed interesting phenomena of microbial biogeography among natural interconnected habitats, suggested that the high interconnectivity reduced the spatial heterogeneity of bacteria, and caused the dispersal of bacteria to be more stochastically. This study has provided a deeper understanding of the biogeographic patterns of rare and abundant bacterial taxa and their determined processes among interconnected aquatic habitats.

microbiology↗

bioRxiv2019

Increased Replication Rates of Dissimilatory Nitrogen-Reducing Bacteria Leads to Decreased Anammox Reactor Performance

BackgroundAnaerobic ammonium oxidation (anammox) is a biological process employed to remove reactive nitrogen from wastewater. While a substantial body of literature describes the performance of anammox bioreactors under various operational conditions and perturbations, few studies have resolved the metabolic roles of their core microbial community members. ResultsHere, we used metagenomics to study the microbial community of a laboratory-scale anammox bioreactor from inoculation, through a performance destabilization event, to robust steady-state performance. Metabolic analyses revealed that nutrient acquisition from the environment is selected for in the anammox community. Dissimilatory nitrate reduction to ammonium (DNRA) was the primary nitrogen removal pathway that competed with anammox. Increased replication of bacteria capable of DNRA led to the out-competition of annamox bacteria, and the loss of the bioreactors nitrogen removal capacity. These bacteria were highly associated with the anammox bacterium and considered part of the core microbial community. ConclusionsOur findings highlight the importance of metabolic interdependencies related to nitrogen- and carbon-cycling within anammox bioreactors and the potentially detrimental effects of bacteria that are otherwise considered core microbial community members.

microbiology↗

bioRxiv2019

Spread of pathological α-synuclein from urogenital nerves initiates multiple system atrophy-like symptoms

Multiple system atrophy (MSA) is a fatal adult-onset movement disorder with autonomic failures, especially urogenital dysfunction. The neuropathological feature of MSA is the accumulation of misfolded -synuclein (-Syn) in the nervous system. Here, we show that misfolded -Syn exist in nerve terminals in detrusor (DET) and external urethral sphincter (EUS) of patients with MSA. Moreover, -Syn preformed fibrils inoculated into the EUS or DET in TgM83+/- mice initiated the transmission of misfolded -Syn from the lower urinary tract to brain, and these mice developed -Syn inclusion pathology through micturition reflex pathways along with urinary dysfunction and motor impairments. These findings indicate that spreading of misfolded -Syn from the autonomic control of the lower urinary tract to the brain via micturition reflex pathways induces autonomic failure and motor impairments. These results provide important new insights into the pathogenesis of MSA as well as highlight potential targets for early detection and therapeutics.

neuroscience↗

bioRxiv2018

Single cell DNA sequencing reveals distinct molecular types of basal cell carcinoma with unique transcriptome features

Background: Aneuploidy, a hallmark of cancer, is the result of chromosomal instability (CIN) during mitosis. While some aneuploid cancers display stable karyotypes, other tumours display cell-to-cell karyotype variability indicative of CIN. CIN cancers are typically associated with poor clinical outcome, as they are endowed with the potential to adjust their genomes to changing conditions including therapy. To further explore this, we assessed the degree of aneuploidy and CIN in basal cell carcinoma (BCC) and investigated whether the karyotypic makeup of tumours was associated with distinct transcriptional responses. Patients and Methods: Samples from 11 BCC patients were processed for single-cell whole genome sequencing (scWGS) to measure aneuploidy and karyotype heterogeneity. In parallel, samples were processed for transcriptome analysis. Results: scWGS revealed different grades of aneuploidy between BCCs, ranging from euploidy to tumours with up to 7 aneusomic chromosomes. Importantly, a subset of BCCs displayed intratumour karyotype heterogeneity, indicating that CIN can play a role in BCC. Samples were clustered into three groups based on the level of aneuploidy and intratumour karyotype heterogeneity. Karyotype-driven group classification was also reflected by the tumour transcriptomes and revealed distinct gene expression signatures related to metabolism for aneuploid BCCs and a DNA damage signature for CIN BCCs. Conclusions: While BCCs are typically classified based on histopathological features, we find that BCCs can be stratified based on karyotypic landscape. Importantly, this classification is linked to distinct molecular features and could thus be the starting point of a molecular classification system for BCC including a readout for CIN. Importantly, the approach that we have developed is broadly applicable and could therefore also improve the diagnosis and treatment of other cancer types.

cancer biology↗

bioRxiv2018

Identification of a putative nuclear localization signal in maspin protein shed light into its nuclear import regulation

Maspin (SERPINB5) is a potential tumor suppressor gene with pleiotropic biological activities, including regulation of cell proliferation, death, adhesion, migration and gene expression. Several studies suggest that subcellular localization plays an essential role on maspin tumor suppression activity. In this study we investigated the molecular mechanisms underlying maspin nucleocytoplasmic shuttling. An in vitro nuclear-import assay using digitonin-permeabilized HeLa cells demonstrated that maspin enters the nucleus by an energy-and carrier-independent mechanism. However, previous studies indicated that maspin subcellular localization is regulated in the cell. Using a nuclear localization signal (NLS) prediction software, we identified a putative NLS in the maspin amino acid sequence. To distinguish between passive and regulated nuclear translocation, maspinNLS or the full-length protein (MaspinFL) were fused to 5GFP, rendering the construct too large to enter the nucleus passively. Unexpectedly, 5GFP-maspinNLS, but not maspinFL-5GFP, entered the nucleus of HeLa cells. Dominant-negative Ran-GTPase mutants RanQ69L or RanT24N, suppressed 5GFP-maspinNLS nuclear localization. In summary, we provide evidence that maspin translocates to the nucleus passively. In addition, we identified a peptide in the maspin protein sequence, which is able to drive a 5GFP construct to the nucleus in an energy-dependent manner.

cell biology↗

bioRxiv2018

Precisely control mitochondrial membrane potential with light to manipulate cell fate decisions

Mitochondrial dysfunction has been implicated in many pathological conditions and diseases. The normal functioning of mitochondria relies on maintaining the inner mitochondrial membrane (IMM) potential (a.k.a. {Delta}{Psi}m) that is essential for ATP synthesis, Ca2+ homeostasis, redox balance and regulation of other key signaling pathways such as mitophagy and apoptosis. However, the detailed mechanisms by which {Delta}{Psi}m regulates cellular function remain incompletely understood, partially due to difficulty of manipulating {Delta}{Psi}m with spatiotemporal resolution, reversibility, or cell type specificity. To address this need, we have developed a next-generation optogenetic-based technique for controllable mitochondrial depolarization with light. We demonstrate successful targeting of the heterologous Channelrhodopsin-2 (ChR2) fusion protein to the IMM and formation of functional cationic channels capable of light-induced selective {Delta}{Psi}m depolarization and mitochondrial autophagy. Importantly, we for the first time show that optogenetic-mediated mitochondrial depolarization can be well-controlled to differentially influence the fate of cells expressing mitochondrial ChR2: while sustained moderate light illumination induces substantial apoptotic cell death, transient mild light illumination elicits cytoprotection via mitochondrial preconditioning. Finally, we show that Parkin overexpression exacerbates, instead of ameliorating, mitochondrial depolarization-mediated cell death in HeLa cells. In summary, we provide evidence that the described mitochondrial-targeted optogenetics may have a broad application for studying the role of mitochondria in regulating cell function and fate decision.

cell biology↗

bioRxiv2018

PP4-dependent HDAC3 dephosphorylation discriminates between axonal regeneration and regenerative failure

The molecular mechanisms discriminating between regenerative failure and success remain elusive. While a regeneration-competent peripheral nerve injury mounts a regenerative gene expression response in bipolar dorsal root ganglia (DRG) sensory neurons, a regeneration-incompetent central spinal cord injury does not. This dichotomic response offers a unique opportunity to investigate the fundamental biological mechanisms underpinning regenerative ability. Following a pharmacological screen with small molecule inhibitors targeting key epigenetic enzymes in DRG neurons we identified HDAC3 signalling as a novel candidate brake to axonal regenerative growth. In vivo, we determined that only a regenerative peripheral but not a central spinal injury induces an increase in calcium, which activates protein phosphatase 4 that in turn dephosphorylates HDAC3 thus impairing its activity and enhancing histone acetylation. Bioinformatics analysis of ex vivo H3K9ac ChIPseq and RNAseq from DRG followed by promoter acetylation and protein expression studies implicated HDAC3 in the regulation of multiple regenerative pathways. Finally, genetic or pharmacological HDAC3 inhibition overcame regenerative failure of sensory axons following spinal cord injury. Together, these data indicate that PP4-dependent HDAC3 dephosphorylation discriminates between axonal regeneration and regenerative failure.\n\n\n\nO_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=122 SRC=\"FIGDIR/small/446963_ufig1.gif\" ALT=\"Figure 1\">\nView larger version (40K):\norg.highwire.dtl.DTLVardef@1bd577corg.highwire.dtl.DTLVardef@1ba990aorg.highwire.dtl.DTLVardef@195813corg.highwire.dtl.DTLVardef@57abc7_HPS_FORMAT_FIGEXP M_FIG Graphical AbstractFollowing central nervous system (CNS) spinal injury, protein phosphatase 4/2 activity is not induced since calcium levels remain unchanged compared to uninjured conditions. HDAC3 remains phosphorylated and occupies deacetylated chromatin contributing to its compaction inhibiting gene expression. Following peripheral nervous system (PNS) sciatic injury, protein phosphatase 4/2 activity is induced by calcium. HDAC3 is dephosphorylated leading to its inhibition and release from chromatin sites contributing to increase in histone acetylation and in the expression of regeneration associated genes (RAGs).\n\nC_FIG

neuroscience↗

bioRxiv2018

Rationally designed mariner vectors to allow functional genomic analysis of Actinobacillus pleuropneumoniae and other bacteria by transposon-directed insertion-site sequencing (TraDIS)

Transposon Directed Insertion Sequencing (TraDIS) is a high-throughput method for mapping insertion sites in large libraries of transposon mutants. The Himar1 (mariner) transposon is ideal for generating near-saturating mutant libraries, especially in AT-rich chromosomes, as the requirement for integration is a TA dinucleotide. In this study, we generated two novel mariner vectors, pTsodCPC9 and pTlacPC9 (differing only in the promoter driving expression of the transposase gene), in order to facilitate TraDIS identification of conditionally essential genes in Actinobacillus pleuropneumoniae and other bacteria. Using the pTlacPC9 vector, we have generated, for the first time, saturating mariner mutant libraries in both A. pleuropneumoniae and Pasteurella multocida that showed a near random distribution of insertions around the respective chromosomes. A preliminary screen of 5000 mutants each identified 8 and 15 genes, respectively, that are required for growth under anaerobic conditions.

microbiology↗

bioRxiv2018

Gata4 drives Hh-signaling for second heart field migration and outflow tract development

Dominant mutations of Gata4, an essential cardiogenic transcription factor (TF), cause outflow tract (OFT) defects in both human and mouse. We investigated the molecular mechanism underlying this requirement. Gata4 happloinsufficiency in mice caused OFT defects including double outlet right ventricle (DORV) and conal ventricular septum defects (VSDs). We found that Gata4 is required within Hedgehog (Hh)-receiving second heart field (SHF) progenitors for normal OFT alignment. Increased Pten-mediated cell-cycle transition, rescued atrial septal defects but not OFT defects in Gata4 heterozygotes. SHF Hh-receiving cells failed to migrate properly into the proximal OFT cushion in Gata4 heterozygote embryos. We find that Hh signaling and Gata4 genetically interact for OFT development. Gata4 and Smo double heterozygotes displayed more severe OFT abnormalities including persistent truncus arteriosus (PTA) whereas restoration of Hedgehog signaling rescued OFT defects in Gata4-mutant mice. In addition, enhanced expression of the Gata6 was observed in the SHF of the Gata4 heterozygotes. These results suggested a SHF regulatory network comprising of Gata4, Gata6 and Hh-signaling for OFT development. This study indicates that Gata4 potentiation of Hh signaling is a general feature of Gata4-mediated cardiac morphogenesis and provides a model for the molecular basis of CHD caused by dominant transcription factor mutations.\n\nAuthor SummaryGata4 is an important protein that controls the development of the heart. Human who possess a single copy of Gata4 mutation display congenital heart defects (CHD), including the double outlet right ventricle (DORV). DORV is an alignment problem in which both the Aorta and Pulmonary Artery originate from the right ventricle, instead of originating from the left and the right ventricles, respectively. To study how Gata4 mutation causes DORV, we used a Gata4 mutant mouse model, which displays DORV. We showed that Gata4 is required in the cardiac precursor cells for the normal alignment of the great arteries. Although Gata4 mutation inhibits the rapid increase in number of the cardiac precursor cells, rescuing this defects does not recover the normal alignment of the great arteries. In addition, there is a movement problem of the cardiac precursor cells when migrating toward the great arteries during development. We further showed that a specific molecular signaling, Hh-signaling, is responsible to the Gata4 action in the cardiac precursor cells. Importantly, over-activating the Hh-signaling rescues the DORV in the Gata4 mutant embryos. This study provides an explanation for the ontogeny of CHD.

developmental biology↗

bioRxiv2018

High-glucose Induces Retinal Pigment Epithelium Mitochondrial Pathways of Apoptosis and Inhibits Mitophagy by Regulating ROS/PINK1/Parkin Signal Pathway

Diabetic retinopathy (DR) caused visual performance degradation seriously endangers human beings health, uncovering the underlying mechanism might shed light on the discovery of DR therapeutic treatments. In this study, we found that the effects of glucose on retinal pigment epithelium (RPE) varies in a dose dependent manner, high-glucose promotes ROS generation and cell apoptosis, inhibits mitophagy as well as proliferative abilities, while low-glucose induces ROS production and cell mitophagy, but has little impacts on cell apoptosis and proliferation. Of note, the toxic effects of high-glucose on RPE are alleviated by ROS scavengers and aggravated by autophagy inhibitor 3-methyladenine (3-MA) or mitophagy inhibitor cyclosporin A (CsA). High-glucose induced ROS generation is merely eliminated by ROS scavengers instead of mitophagy or autophagy inhibitor. We also proved that high-glucose inhibits cell proliferation and promotes cell apoptosis by regulating ROS mediated inhibition of mitophagy. In addition, mitophagy associated proteins PINK1 and Parkin are downregulated by high-glucose or hydrogen peroxide treatments, which are reversed by ROS scavengers. Of note, Knock-down of PINK1 decreases phospharylated Parkin instead of total Parkin levels in RPE. Intriguingly, high-glucoses inhibiting effects on cell mitophagy as well as proliferation and its promoting effects on cell apoptosis are reversed by either PINK1 or Parkin overexpression. Therefore, we concluded that high-glucose promotes RPE apoptosis and inhibits cell proliferation as well as mitophagy by regulating oxidative stress mediated inactivation of ROS/PINKl/Parkin signal pathway.

cell biology↗

bioRxiv2018

Developmental heterogeneity of microglia and brain myeloid cells revealed by deep single-cell RNA sequencing

Microglia are increasingly recognized for their major contributions during brain development and neurodegenerative disease. It is currently unknown if these functions are carried out by subsets of microglia during different stages of development and adulthood or within specific brain regions. Here, we performed deep single-cell RNA sequencing (scRNA-seq) of microglia and related myeloid cells sorted from various regions of embryonic, postnatal, and adult mouse brains. We found that the majority of adult microglia with homeostatic signatures are remarkably similar in transcriptomes, regardless of brain region. By contrast, postnatal microglia represent a more heterogeneous population. We discovered that postnatal white matter-associated microglia (WAM) are strikingly different from microglia in other regions and express genes enriched in degenerative disease-associated microglia. These postnatal WAM have distinct amoeboid morphology, are metabolically active, and phagocytose newly formed oligodendrocytes. This scRNA-seq atlas will be a valuable resource for dissecting innate immune functions in health and disease.\n\nHighlightsO_LIMyeloid scRNA-seq atlas across brain regions and developmental stages\nC_LIO_LILimited transcriptomic heterogeneity of homeostatic microglia in the adult brain\nC_LIO_LIPhase-specific gene sets of proliferating microglia along cell cycle pseudotime\nC_LIO_LIPhagocytic postnatal white matter-associated microglia sharing DAM gene signatures\nC_LI

neuroscience↗

bioRxiv2018

Efficient Multivariate Analysis Algorithms for Longitudinal Genome-wide Association Studies

MotivationCurrent dynamic phenotyping system introduces time as an extra dimension to genome-wide association studies (GWAS), which helps to explore the mechanism of dynamical genetic control for complex longitudinal traits. However, existing methods for longitudinal GWAS either ignore the covariance among observations of different time points or encounter computational efficiency issues.\n\nResultsWe herein developed efficient genome-wide multivariate association algorithms (GMA) for longitudinal data. In contrast to existing univariate linear mixed model analyses, the proposed new method has improved statistic power for association detection and computational speed. In addition, the new method can analyze unbalanced longitudinal data with thousands of individuals and more than ten thousand records within a few hours. The corresponding time for balanced longitudinal data is just a few minutes.\n\nAvailability and ImplementationWe wrote a software package to implement the efficient algorithm named GMA (https://github.com/chaoning/GMA), which is available freely for interested users in relevant fields.

bioinformatics↗

bioRxiv2018

Effective principal components analysis of SNP data

PCA is frequently used to display and discover patterns in SNP data from humans, animals, plants, and microbes--especially to elucidate population structure. Given the popularity of PCA, one might expect that PCA is understood well and applied effectively. However, our literature survey of 125 representative articles that apply PCA to SNP data shows that three choices have usually been made poorly: SNP coding, PCA variant, and PCA graph. Accordingly, we offer several simple recommendations for effective PCA analysis of SNP data. The ultimate benefit from informed and optimal choices of SNP coding, PCA variant, and PCA graph is expected to be discovery of more biology, and thereby acceleration of medical, agricultural, and other vital applications.

genomics↗

bioRxiv2018

Heterodimerization of UNC-13/RIM regulates synaptic vesicle release probability but not priming

UNC-13 proteins play an essential role in synaptic transmission by recruiting synaptic vesicles (SVs) to become available for release, which is termed SV priming. Here we show that the C2A domain of UNC-13L, like the corresponding domain in mammalian Munc13-1, displays two conserved binding modes: forming C2A/C2A homodimers, or forming a heterodimer with the zinc finger domain of UNC-10/RIM (C2A/RIM). Functional analysis revealed that UNC-13Ls C2A promotes synaptic transmission by regulating a post-priming process. Stimulus-evoked release but not SV priming, was impaired in unc-10 mutants deficient for C2A/RIM heterodimerization, leading to decreased release probability. Disrupting C2A/C2A homodimerization in UNC-13L-rescued animals had no effect on synaptic transmission, but fully restored the evoked release and the release probability of unc-10/RIM mutants deficient for C2A/RIM heterodimerization. Thus, our results support the model that RIM binding C2A releases UNC-13L from an autoinhibitory homodimeric complex to become fusion-competent by functioning as a switch only.

neuroscience↗

bioRxiv2018

Detection of cellular microRNAs with programmable DNA nanoswitches

MicroRNAs are short non-coding regulatory RNAs that are increasingly used as disease biomarkers. Detection of microRNAs can be arduous and expensive, and often requires amplification, labeling, or radioactive probes. Here we report a single-step, non-enzymatic detection assay using conformationally responsive DNA nanoswitches. Termed miRacles (microRNA activated conditional looping of engineered switches), our assay has sub-attomole sensitivity and single-nucleotide specificity using an agarose gel electrophoresis readout. We detect cellular microRNAs from nanogram-scale RNA extracts of differentiating muscle cells, and demonstrate multiplexed detection of several microRNAs from one biological sample. We demonstrate one-hour detection without expensive equipment or reagents, making this assay a compelling alternative to qPCR and Northern blotting.\n\nSignificance statementDetection of microRNAs play a key role in biological research and medical diagnostics, and current detection methods are expensive and require sophisticated processes. We present microRNA activated conditional looping of engineered switches (miRacles), a mix-and-read strategy that is based on conformational changes of DNA nanoswitches upon binding a target microRNA. MiRacles has a sensitivity of [~]4 copies/cell and specificity of a single nucleotide, and can be performed in one hour at a fraction of the cost of traditional microRNA detection techniques. Our method can also be multiplexed to detect multiple microRNAs from one biological sample. The minimalistic miRacles assay has immediate application in biomedical research and longer term potential as a clinical tool.

bioengineering↗

bioRxiv2018

Inward tubulation of the plasma membrane expedites membrane exchange and receptor presentation

The plasma membrane is a crucial barrier between the cell and its external environment, and it also enables efficient passage of materials and information. Membrane vesicle trafficking allows precise delivery of materials but is rather inefficient. The mechanism for efficient membrane exchange remains elusive. Here we describe inward tubulation of the plasma membrane (PM tubes) that extends deep into the cytoplasm. These widespread PM tubes elongate along microtubules and are stabilized by actin filaments and cholesterol. PM tubes are preferred sites for connection between the endoplasmic reticulum and the plasma membrane. PM tubes facilitate receptor presentation at the surface of cells, possibly also shortening the distance for transported cargo to reach the external environment.\n\nIn BriefA new type of tubular membrane structures was discovered in cells, revealing a shortcut that cells employ to expedite material exchange with their external environment.\n\nHighlightsO_LIInward tubulation of the plasma membrane (PM tubes), transiently interacts with the Golgi apparatus\nC_LIO_LIMicrotubule side-binding proteins pull PM tubes, while actin filaments and cholesterol stabilize PM tubes\nC_LIO_LIPM tubes are preferred sites where ER-PM contacts form in response to increased cytoplasmic calcium concentration\nC_LIO_LIPM tubes are preferred sites for the surface presentation of GLUT1 upon glucose deprivation\nC_LI

cell biology↗

bioRxiv2018

A Cut/cohesin axis alters the chromatin landscape to facilitate neuroblast death

Precise control of cell death in the nervous system is essential for development. Spatial and temporal factors activate the death of Drosophila neural stem cells (neuroblasts) by controlling the transcription of multiple cell death genes through a shared enhancer, enh1. The activity of enh1 is controlled by abdominalA and Notch, but additional inputs are needed for proper specificity. Here we show that the Cut DNA binding protein is required for neuroblast death, acting downstream of enh1. In the nervous system, Cut promotes an open chromatin conformation in the cell death gene locus, allowing cell death gene expression in response to abdominalA. We demonstrate a temporal increase in global H3K27me3 levels in neuroblasts, which is enhanced by cut knockdown. Furthermore, cut regulates the expression of the cohesin subunit Stromalin in the nervous system. The cohesin components Stromalin and NippedB are required for neuroblast death, and knockdown of Stromalin increases repressive histone modifications in neuroblasts. Thus Cut and cohesin regulate apoptosis in the developing nervous system by altering the chromatin landscape.\n\nSummary statementCut regulates the programmed death of neural stem cells by altering cohesin levels and promoting a more open chromatin conformation to allow cell death gene expression.

developmental biology↗

bioRxiv2018

Genetic analysis using parent-progeny relationship for wood quality traits in Norway spruce (Picea abies (L.) Karst.)

Two-generations pedigree involving 524 plus trees and their open-pollinated (OP) progenies were jointly studied to estimate parent-progeny correlation and heritability. Three wood traits (wood density, MFA, and MOE) were determined by SilviS-can in one ramet per plus tree and 12 OP progenies. Three ramets per plus tree and 12 OP were also measured with two indirect methods, Pilodyn and Hitman. The overall correlation between OP-based breeding values and plus tree-based phenotypes was low to moderate for all traits. The correlations between the phenotypic values of the mother trees and the breeding values estimated on their half-sib pro-genies are low to moderate. Reasons for this may be experimental errors in progeny trials and lack of experimental design in archives, contributing to the parent and progeny correlation. The management practices in the archive may contribute more to such low correlation. Offspring progeny heritability estimates based on SilviScan measurements were higher than parent-offspring regression using one single ramet from the archive. Moreover, when three ramets were measured the parent-offspring regression heritability estimates were higher than those based solely on progeny data for the Pilodyn and Hitman on the standing trees. The standard error of the heritability estimates decreased with increasing progeny size.

plant biology↗