Cannabis sativa is a well-known plant species that has great economic and ecological significance. An incomplete genome of cloned C. sativa was obtained by using SOAPdenovo software in 2011. To further explore the utilization of this plant resource, we generated an updated draft genome sequence for wild-type varieties of C. sativa in China using PacBio single-molecule sequencing and Hi-C technology. Our assembled genome is approximately 808 Mb, with scaffold and contig N50 sizes of 83.00 Mb and 513.57 kb, respectively. Repetitive elements account for 74.75% of the genome. A total of 38,828 protein-coding genes were annotated, 98.20% of which were functionally annotated. We provide the first comprehensive de novo genome of wild-type varieties of C. sativa distributed in Tibet, China. Due to long-term growth in the wild environment, these varieties exhibit higher heterozygosity and contain more genetic information. This genetic resource is of great value for future investigations of cannabinoid metabolic pathways and will aid in promoting the commercial production of C. sativa and the effective utilization of cannabinoids. The assembled genome is also a valuable resource for intensively and effectively investigating the C. sativa genome further in the future.

Several plant lipid transfer proteins (LTPs) act positively in plant disease resistance. Here, we show that LTP3 (At5g59320), a pathogen and abscisic acid (ABA)-induced gene, negatively regulates plant immunity in Arabidopsis. The overexpression of LTP3 (LTP3-OX) led to an enhanced susceptibility to virulent bacteria and compromised resistance to avirulent bacteria. On infection of LTP3-OX plants with Pseudomonas syringae pv. tomato, genes involved in ABA biosynthesis, NCED3 and AAO3, were highly induced, whereas salicylic acid (SA)-related genes, ICS1 and PR1, were down-regulated. Accordingly, in LTP3-OX plants, we observed increased ABA levels and decreased SA levels relative to the wild-type. We also showed that the LTP3 overexpression-mediated enhanced susceptibility was partially dependent on AAO3. Interestingly, loss of function of LTP3 (ltp3-1) did not affect ABA pathways, but resulted in PR1 gene induction and elevated SA levels, suggesting that LTP3 can negatively regulate SA in an ABA-independent manner. However, a double mutant consisting of ltp3-1 and silent LTP4 (ltp3/ltp4) showed reduced susceptibility to Pseudomonas and down-regulation of ABA biosynthesis genes, suggesting that LTP3 acts in a redundant manner with its closest homologue LTP4 by modulating the ABA pathway. Taken together, our data show that LTP3 is a novel negative regulator of plant immunity which acts through the manipulation of the ABA-SA balance.