No abstract

The mangrove Kandelia obovata (Rhizophoraceae) is an important coastal shelterbelt and landscape tree distributed in tropical and subtropical areas across East Asia and Southeast Asia. Herein, a chromosome-level reference genome of K. obovata based on PacBio, Illumina, and Hi-C data is reported. The high-quality assembled genome size is 177.99 Mb, with a contig N50 value of 5.74 Mb. A large number of contracted gene families and a small number of expanded gene families, as well as a small number of repeated sequences, may account for the small K. obovata genome. We found that K. obovata experienced two whole-genome polyploidization events: one whole-genome duplication shared with other Rhizophoreae and one shared with most eudicots (γ event). We confidently annotated 19,138 protein-coding genes in K. obovata and identified the MADS-box gene class and the RPW8 gene class, which might be related to flowering and resistance to powdery mildew in K. obovata and Rhizophora apiculata, respectively. The reference K. obovata genome described here will be very useful for further molecular elucidation of various traits, the breeding of this coastal shelterbelt species, and evolutionary studies with related taxa.

No abstract

The IFT-B complex mediates ciliary anterograde protein trafficking and membrane protein export together with the BBSome. Bardet-Biedl syndrome (BBS) is caused by mutations in not only all BBSome subunits, but also in some IFT-B subunits, including IFT74/BBS22 and IFT27/BBS19, which form heterodimers with IFT81 and IFT25, respectively. We found that the IFT25–IFT27 dimer bind the C-terminal region of the IFT74–IFT81 dimer, and that the IFT25–IFT27-binding region encompasses the region deleted in the BBS variants of IFT74. In addition, we found that the missense BBS variants of IFT27 are impaired in IFT74–IFT81 binding, and are unable to rescue the BBS-like phenotypes of IFT27-knockout cells. Furthermore, the BBS variants of IFT74 rescued the ciliogenesis defect of IFT74-knockout cells, but the rescued cells demonstrated BBS-like abnormal phenotypes. Taken together, we conclude that the impaired interaction between IFT74–IFT81 and IFT25–IFT27 causes the BBS-associated ciliary defects.