植物胚乳发育的表观遗传学调控

被子植物的种子发育从双受精开始, 产生二倍体的胚和三倍体的胚乳。在种子发育和萌发过程中, 胚乳向胚组织提供营养物质, 因此胚乳对胚和种子的正常生长发育至关重要。开花植物发生基因组印迹的主要器官是胚乳。印迹基因的表达受表观遗传学机制的调控, 包括DNA甲基化和组蛋白H3K27甲基化修饰以及依赖于PolIV的siRNAs (p4-siRNAs)调控。基因组印迹的表观遗传学调控对胚乳的正常发育和种子育性具有不可或缺的重要作用。最新研究显示, 胚乳的整个基因组DNA甲基化水平降低, 而且去甲基化作用可能源于雌配子体的中央细胞。该文综述了种子发育的表观遗传学调控机制, 包括基因组印迹机制以及胚乳基因组DNA甲基化变化研究的最新进展。     

Jaatha: a fast composite-likelihood approach to estimate demographic parameters

While information about a species’ demography is interesting in its own right, it is an absolute necessity for certain types of population genetic analyses. The most widely used methods to infer a species’ demographic history do not take intralocus recombination or recent divergence into account, and some methods take several weeks to converge. Here, we present Jaatha, a new composite‐likelihood method that does incorporate recent divergence and is also applicable when intralocus recombination rates are high. This new method estimates four demographic parameters. The accuracy of Jaatha is comparable to that of other currently available methods, although it is superior under certain conditions, especially when divergence is very recent. As a proof of concept, we apply this new method to estimate demographic parameters for two closely related wild tomato species, Solanum chilense and S. peruvianum. Our results indicate that these species likely diverged 1.44·N generations ago, where N is the effective population size of S. chilense, and that some introgression between these species continued after the divergence process initiated. Furthermore, S. peruvianum likely experienced a population expansion following speciation.     

Genomic imprinting and endosperm development in flowering plants

Genomic imprinting, the parent-of-origin-specific expression of genes, plays an important role in the seed development of flowering plants. As different sets of genes are imprinted and hence silenced in maternal and paternal gametophyte genomes, the contributions of the parental genomes to the offspring are not equal. Imbalance between paternally and maternally imprinted genes, for instance as a result of interploidy crosses, or in seeds in which imprinting has been manipulated, results in aberrant seed development. It is predominantly the endosperm, and not or to a far lesser extent the embryo, that is affected by such imbalance. Deviation from the normal 2m:1p ratio in the endosperm genome has a severe effect on endosperm development, and often leads to seed abortion. Molecular expression data for imprinted genes suggest that genomic imprinting takes place only in the endosperm of the developing seed. Although far from complete, a picture of how imprinting operates in flowering plants has begun to emerge. Imprinted genes on either the maternal or paternal side are marked and silenced in a process involving DNA methylation and chromatin condensation. In addition, on the maternal side, imprinted genes are most probably under control of the polycomb FIS genes.     

When genomes collide: aberrant seed development following maize interploidy crosses

Background and Aims: The results of wide- or interploidy crosses in angiosperms areunpredictable and often lead to seed abortion. The consequencesof reciprocal interploidy crosses have been explored in maizein detail, focusing on alterations to tissue domains in themaize endosperm, and changes in endosperm-specific gene expression. Methods: Following reciprocal interploidy crosses between diploid andtetraploid maize lines, development of endosperm domains wasstudied using GUS reporter lines, and gene expression in resultingkernels was investigated using semi-quantitative RT-PCR on endospermsisolated at different stages of development. Key Results: Reciprocal interploidy crosses result in very small, largelyinfertile seeds with defective endosperms. Seeds with maternalgenomic excess are smaller than those with paternal genomicexcess, their endosperms cellularize earlier and they accumulatesignificant quantities of starch. Endosperms from the reciprocalcross undergo an extended period of cell proliferation, andaccumulate little starch. Analysis of reporter lines and geneexpression studies confirm that functional domains of the endospermare severely disrupted, and are modified differently accordingto the direction of the interploidy cross. Conclusions: Interploidy crosses affect factors which regulate the balancebetween cell proliferation and cell differentiation within theendosperm. In particular, unbalanced crosses in maize affecttransfer cell differentiation, and lead to the temporal deregulationof the ontogenic programme of endosperm development.     

Structural Analysis of the Interactions Between Hsp70 Chaperones and the Yeast DNA Replication Protein Orc4p

Hsp70 chaperones, besides their role in assisting protein folding, are key modulators of protein disaggregation, being consistently found as components of most macromolecular assemblies isolated in proteome-wide affinity purifications. A wealth of structural information has been recently acquired on Hsp70s complexed with Hsp40 and NEF co-factors and with small hydrophobic target peptides. However, knowledge of how Hsp70s recognize large protein substrates is still limited. Earlier, we reported that homologue Hsp70 chaperones (DnaK in Escherichia coli and Ssa1-4p/Ssb1-2p in Saccharomyces cerevisiae) bind strongly, both in vitro and in vivo, to the AAA+ domain in the Orc4p subunit of yeast origin recognition complex (ORC). ScORC is the paradigm for eukaryotic DNA replication initiators and consists of six distinct protein subunits (ScOrc1p-ScOrc 6p). Here, we report that a hydrophobic sequence (IL₄) in the initiator specific motif (ISM) in Orc4p is the main target for DnaK/Hsp70. The three-dimensional electron microscopy reconstruction of a stable Orc4p₂-DnaK complex suggests that the C-terminal substrate-binding domain in the chaperone clamps the AAA+ IL₄ motif in one Orc4p molecule, with the substrate-binding domain lid subdomain wedging apart the other Orc4p subunit. Pairwise co-expression in E. coli shows that Orc4p interacts with Orc1/2/5p. Mutation of IL₄ selectively disrupts Orc4p interaction with Orc2p. Allelic substitution of ORC4 by mutants in each residue of IL₄ results in lethal (I184A) or thermosensitive (L185A and L186A) initiation-defective phenotypes in vivo. The interplay between Hsp70 chaperones and the Orc4p-IL₄ motif might have an adaptor role in the sequential, stoichiometric assembly of ScORC subunits.