Plant-associated microbiomes are key determinants of host-plant fitness, productivity, and function. However, compared to bacterial community, we still lack fundamental knowledge concerning the variation in the fungal microbiome at the plant niche level. In this study, we quantified the fungal communities in the rhizosphere soil, as well as leaf and root endosphere compartments of a subtropical island shrub, Mussaenda kwangtungensis , using high-throughput DNA sequencing. We found that fungal microbiomes varied significantly across different plant compartments. Rhizosphere soil exhibited the highest level of fungal diversity, whereas the lowest level was found in the leaf endosphere. Further, the fungal communities inhabiting the root endosphere shared a greater proportion of fungal operational taxonomic units (OTUs) with rhizosphere communities than with leaf fungal endophyte communities, despite significant separation in community structure between the two belowground compartments. The fungal co-occurrence networks in the three compartments of M. kwangtungensis showed scale-free features and non-random co-occurrence patterns and matched the topological properties of small-world and evidently modular structure. Additionally, the rhizosphere network was more complex and showed higher centrality and connectedness than the leaf and root endosphere networks. Overall, our findings provide comprehensive insights into the structural variability, niche differentiation, and co-occurrence patterns in the plant associated fungal microbiome.
Reproductive systems of flowering plants are evolutionarily fluid, with mating patterns changing in response to shifts in abiotic conditions, pollination systems, and population characteristics. Changes in mating should be particularly evident in species with sexual polymorphisms that become ecologically destabilized, promoting transitions to alternative reproductive systems. Here, we decompose female mating portfolios (incidence of selfing, outcross mate number, and intermorph mating) in eight populations of Primula oreodoxa, a self-compatible insect-pollinated herb. This species is ancestrally distylous, with populations subdivided into two floral morphs that usually mate with each other (disassortative mating). Stages in the breakdown of polymorphism also occur, including “mixed” populations of distylous and homostylous (self-pollinating) morphs and purely homostylous populations. Population morph ratios vary with elevation in association with differences in pollinator availability, providing an unusual opportunity to investigate changes in mating patterns accompanying transitions in reproductive systems. Unexpectedly, individuals mostly outcrossed randomly, with substantial disassortative mating in at most two distylous populations. As predicted, mixed populations had higher selfing rates than distylous populations, within mixed populations, homostyles selfed almost twice as much as the distylous morphs, and homostylous populations exhibited the highest selfing rates. Populations with homostyles outcrossed with fewer mates and mate number varied negatively with population selfing rates. These differences indicate maintenance of distyly at low elevation, transition to monomorphic selfing at high elevation, and uncertain, possibly variable fates at intermediate elevation. By quantifying the earliest changes in mating that initiate reproductive transitions, our study highlights the key role of mating in promoting evolutionary divergence.
Joubert syndrome (JS) is an autosomal recessive disorder, which is characterized by hypotonia, ataxia, psychomotor delay, and variable occurrences of oculomotor apraxia and neonatal breathing abnormalities. JS is clinically and genetically heterogeneous. The present study investigated a typical JS family. The 'molar tooth sign' was observed in the proband through magnetic resonance imaging. Other symptoms of JS include cerebellar vermis hypoplasia/dysplasia, oculomotor apraxia and intellectual disability. High‑throughput sequencing revealed that JS was caused by coiled‑coil and C2 domain containing 2A (CC2D2A) compound heterozygous mutations. One CC2D2A allele was affected with a missense mutation, c.2581G>A, which led to a p.Asp861Asn amino acid replacement. The other allele was affected with a c.2848C>T nonsense mutation, which resulted in a truncated CC2D2A protein (p.Arg950Ter). Both of these alterations are novel. Further investigation indicated that the proband's father was the c.2581G>A carrier, whereas the mother was the c.2848C>T carrier. These results indicated that JS in the proband was caused by novel compound heterozygous mutations in CC2D2A, which were inherited from both parents. These findings may be used to establish prenatal molecular diagnostic criteria, which may be beneficial in future pregnancies.
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