A 2.09 Mb fragment translocation on chromosome 6 causes abnormalities during meiosis and leads to less seed watermelon

Seedlessness is a valuable agronomic trait in watermelon(Citrullus lanatus)breeding.Conventional less seed watermelons are mainly triploid,which has many disadvantages due to unbalanced genome content.Less seed watermelon can be achieved at the diploid level when certain reproductive genes are mutated or by chromosome translocation,which leads to defects during meiosis.However,the formation mechanism of diploid less seed watermelons remains largely unknown.Here,we identified a spontaneous mutant line,watermelon line“148”,which can set seeds normally when self-pollinated.A total of 148×JM F_(1) hybrid plants exhibited seed number reductions to 50.3%and 47.3%of those of the two parental lines,respectively,which are considered to be less seed.Examination of pollen viability and hybridization experiments revealed that F 1 hybrids produce semisterile pollen and ovules.Further cytological observations indicated that semisterility was a result of a reciprocal translocation of chromosomes,which exhibited one quadrivalent ring of four chromosomes at prometaphase I during meiosis.RT-qPCR analysis indirectly confirmed that the semisterile phenotype is caused by chromosome translocation rather than disruption of specific meiotic gene expression.F 2 population genetic analysis indicated that the“148”watermelon line is a homozygous translocation and that the less seed phenotype of the F_(1) hybrid is prompted by one chromosome fragment translocation.The translocated fragment was further fine mapped to a 2.09 Mb region on chromosome 6 by whole-genome resequencing and genetic map cloning procedures.Our work revealed that a 2.09Mb chromosome fragment translocation on chromosome 6,causing meiotic defects at metaphase I during meiosis,leads to diploid less seed watermelon.Our findings provide a new promising method for less seed watermelon breeding at the diploid level,as well as a fragment size reference for breeding less seed watermelon through artificially induced chromosome translocation.

AtRKD5 inhibits the parthenogenic potential mediated by AtBBM

Parthenogenesis,the development of unfertilized egg cells into embryos,is a key component of apomixis.AtBBM(BABY BOOM),a crucial regulator of embryogenesis in Arabidopsis,possesses the capacity to shift nutritional growth toward reproductive growth.However,the mechanisms underlying AtBBM-induced parthenogenesis remain largely unexplored in dicot plants.Our findings revealed that in order to uphold the order of sexual reproduction,the embryo-specific promoter activity of AtBBM as well as repressors that inhibit its expression in egg cells combine to limiting its ability to induce parthenogenesis.Notably,AtRKD5,a RWPRK domain-containing(RKD)transcription factor,binds to the 3'end of AtBBM and is identified as one of the inhibitory factors for AtBBM expression in the egg cell.In the atrkd5 mutant,we successfully achieved enhanced ectopic expression of AtBBM in egg cells,resulting in the generation of haploid offspring via parthenogenesis at a rate of 0.28%.Furthermore,by introducing chimeric Arabidopsis and rice BBM genes into the egg cell,we achieved a significant 4.6-fold enhancement in haploid induction through the atdmp8/9 mutant.These findings lay a strong foundation for further exploration of the BBM-mediated parthenogenesis mechanism and the improvement of haploid breeding efficiency mediated by the dmp8/9 mutant.