Multiple plant lineages have independently evolved sex chromosomes and variable karyotypes to maintain their sessile lifestyles through constant biological innovation. Morus notabilis, a dioecious mulberry species, has the fewest chromosomes among Morus spp., but the genetic basis of sex determination and karyotype evolution in this species has not been identified. In this study, three high-quality genome assemblies were generated for Morus spp. [including dioecious M. notabilis (male and female) and Morus yunnanensis (female)] with genome sizes of 301–329 Mb and were grouped into six pseudochromosomes. Using a combination of genomic approaches, we found that the putative ancestral karyotype of Morus species was close to 14 protochromosomes, and that several chromosome fusion events resulted in descending dysploidy (2n = 2x = 12). We also characterized a ∼ 6.2-Mb sex-determining region on chromosome 3. Four potential male-specific genes, a partially duplicated DNA helicase gene (named MSDH) and three Ty3_Gypsy long terminal repeat retrotransposons (named MSTG1/2/3), were identified in the Y-linked area and considered to be strong candidate genes for sex determination or differentiation. Population genomic analysis showed that Guangdong accessions in China were genetically similar to Japanese accessions of mulberry. In addition, genomic areas containing selective sweeps that distinguish domesticated mulberry from wild populations in terms of flowering and disease resistance were identified. Our study provides an important genetic resource for sex identification research and molecular breeding in mulberry.
Ciboria shiraiana causes hypertrophy sorosis scleroteniosis in mulberry trees resulting in huge economic losses, and exploring its pathogenic mechanism at genomic level is important to develop new control methods. Here, genome sequencing of C. shiraiana based on PacBio RSII and Illumina HiSeq 2500 platform as well as manual gap filling was performed. Synteny analysis with Sclerotinia sclerotiorum revealed 16 putative chromosomes corresponding to 16 chromosomes of C. shiraiana. Screening of rapid evolution genes revealed that 97% and 2.4% of genes had undergone purifying selection and positive selection, respectively. When compared with S. sclerotiorum, fewer secreted effector proteins were found in C. shiraiana. The number of genes involved in pathogenicity, including secondary metabolites, CAZymes, and P450s, in C. shiraiana genome was comparable to that of other necrotrophs, but higher than that of biotrophs and saprotrophs. The growth-related genes and plant cell wall degradation related genes in C. shiraiana were expressed in different developmental and infection stages, and may be potential targets for prevention and control of this pathogen. These results provide new insights into C. shiraiana pathogenic mechanisms, especially host range and necrotrophy features, and lay foundation for further study on the underlying molecular mechanisms.
Regulator of G-protein signaling (RGS) protein, the best-characterized accelerating GTPase protein in plants, regulates G-protein signaling and plays important role in abiotic stress tolerance. However, the detailed molecular mechanism of RGS involved in G-protein signaling mediated abiotic stress responses remains unclear. In this study, a mulberry (Morus alba L.) RGS gene (MaRGS) was transformed into tobacco, and the ectopic expression of MaRGS in tobacco decreased the tolerance to salt stress. The transgenic tobacco plants had lower proline content, higher malonaldehyde and H 2 O 2 contents than wild type plants under salt stress condition. Meanwhile, MaRGS overexpression in mulberry seedlings enhances the sensitivity to salt stress and RNAi-silenced expression of MaRGS improves the salt stress response and tolerance. These results suggested that MaRGS negatively regulates salt stress tolerance. Further analysis suggested that D-glucose and autophagy may involve in the response of RGS to salt stress. This study revealed the role of MaRGS in salt stress tolerance and provides a proposed model for RGS regulates G-protein signaling in response to salt stress.
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