Biology subjects

Du, Q.

Publications and source records attributed to Du, Q..

4 recordsLinked to original sources

bioRxiv2018

Maize EHD1 is Required for Kernel Development and Vegetative Growth through Regulating Auxin Homeostasis

The roles of EHDs in clathrin-mediated endocytosis (CME) in plants are poorly understood. Here, we isolated a maize mutant, designated as ehd1, which showed defects in kernel development and vegetative growth. Positional cloning and transgenic analysis revealed that ehd1 encodes an EHD protein. Internalization of the endocytic tracer FM4-64 was significantly reduced in ehd1 mutant and ZmEHD1 knock-out mutants. We further demonstrated that ZmEHD1 and ZmAP2 {sigma} subunit physically interact in the plasma membranes. Cellular IAA levels were significantly lower in ehd1 mutant than in wild-type maize. Auxin distribution and ZmPIN1a-YFP localization were altered in ehd1 mutant. Exogenous application of 1-NAA but not GA3 rescued the seed germination and seedling emergency phenotypic defects of ehd1 mutants. Taken together, these results indicate that ZmEHD1 regulates auxin homeostasis by mediating CME through its interaction with the ZmAP2 {sigma} subunit, which is crucial for kernel development and vegetative growth of maize.

plant biology↗

bioRxiv2018

Using LASSO in gene co-expression network for genome-wide identification of gene interactions responding to salt stress in rice

In many applications, such as gene co-expression network analyses, data arises with a huge number of covariates while the size of sample is comparatively small. To improve the accuracy of prediction, variable selection is often used to get a sparse solution by forcing coefficients of variables contributing less to the observed response variable to zero. Various algorithms were developed for variable selection, but LASSO is well known for its statistical accuracy, computational feasibility and broad applicability to adaptation. In this project, we applied LASSO to the gene co-expression network of rice with salt stress to discover key gene interactions for salt-tolerance related phenotypes. The dataset we have is a high-dimensional one, having 50K genes from 100 samples, with the issue of multicollinearity for fitting linear regression - the expression level of genes in the same pathway tends to be highly correlated. The property of LASSO with sparse parameters is naturally suitable to identify gene interactions of interest in this dataset. After biologically functional modules in the co-expression network was identified, the major changed expression patterns were further selected by LASSO regression to establish a linear relationship between gene expression profiles and physiological responses, such as sodium/potassium condenses, with salt stress. Five modules of intensively co-expressed genes, from 45 to 291 genes, were identified by our method with significant P-values, which indicate these modules are significantly associated with physiological responses to stress. Genes in these modules have functions related to ion transport, osmotic adjustment, and oxidative tolerance. For example, LOC_Os7g47350 and LOC_Os07g37320 are co-expressed gene in the same module 15. Both are ion transporter genes and have higher gene expression levels for rice with low sodium levels with salt stress.

bioinformatics↗

bioRxiv2018

Par3 regulates Rac1 signaling and microtubule organization during planar polarization of auditory hair cells

In the inner ear sensory epithelia, hair bundles atop sensory hair cells are mechanosensory apparati with planar polarized structure and orientation. This is established during development by the concerted action of tissue-level planar cell polarity (PCP) signaling and a hair cell-intrinsic, microtubule-mediated machinery. However, how various polarity signals are integrated during hair bundle morphogenesis is poorly understood. Here, we show that the conserved cell polarity protein Par3 plays a key role in planar polarization of hair cells. Par3 deletion in the inner ear resulted in defects in cochlear length, hair bundle orientation and kinocilium positioning. During PCP establishment, Par3 promotes localized Rac-Pak signaling through an interaction with Tiam1. Par3 regulates microtubule dynamics and organization, which is crucial for basal body positioning. Moreover, there is reciprocal regulation of Par3 and the core PCP molecule Vangl2. Thus, we conclude that Par3 is an effector and integrator of cell-intrinsic and tissue-level PCP signaling.\n\nOne sentence summaryPar3 regulates planar polarity of auditory hair cells

developmental biology↗

bioRxiv2018

Replication timing shapes the cancer epigenome and the nature of chromosomal rearrangements

HighlightsO_LIReplication timing alterations are conserved in cancers of different cell origins\nC_LIO_LILong-range epigenetic deregulation in cancer involves altered replication timing\nC_LIO_LICancer late-replicating loci are hypomethylated and acquire facultative heterochromatin\nC_LIO_LIReplication timing status potentiates cis and trans chromosomal rearrangements\nC_LI\n\nSummaryReplication timing is known to facilitate the establishment of epigenome, however, the intimate connection between DNA replication timing and changes to the genome and epigenome in cancer remain uncharted. Here, we perform Repli-Seq and integrated epigenome analysis and show that early-replicating loci are predisposed to hypermethylation and late-replicating loci to hypomethylation, enrichment of H3K27me3 and concomitant loss of H3K9me3. We find that altered replication timing domains correspond to long-range epigenetically deregulated regions in prostate cancer, and a subset of these domains are remarkably conserved across cancers from different tissue origins. Analyses of 214 prostate and 35 breast cancer genomes reveal that late-replicating DNA is prone to cis and early-replicating DNA to trans chromosomal rearrangements. We propose that differences in epigenetic deregulation related to spatial and temporal positioning between early and late replication potentiate the landscape of chromosomal rearrangements in cancer.

genomics↗