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Background  The shedding of premature sweet cherry ( Prunus avium  L) fruitlet has significantly impacted production, which in turn has a consequential effect on economic benefits.    Result  To better understand the molecular mechanism of sweet cherry fruitlet abscission, pollen viability and structure had been observed from the pollination trees. Subsequently, the morphological characters of the shedding fruitlet, the plant hormone titers of dropping carpopodium, the transcriptome of the abscising carpopodium, as well as the HD-ZIP gene family were investigated. These findings showed that the pollens giving rise to heavy fruitlet abscission were malformed in structure, and their viability was lower than the average level. The abscising fruitlet and carpopodium were characterized in red color, and embryos of abscising fruitlet were aborted, which was highly ascribed to the low pollen viability and malformation. Transcriptome analysis showed 6462 were significantly differentially expressed, of which 2456 genes were up-regulated and 4006 down-regulated in the abscising carpopodium. Among these genes, the auxin biosynthesis and signal transduction genes ( α-Trp ,  AUX1 ), were down-regulated, while the 1-aminocyclopropane-1-carboxylate oxidase gene ( ACO ) affected in ethylene biosynthesis, was up-regulated in abscising carpopodium. About genes related to cell wall remodeling ( CEL ,  PAL ,  PG EXP ,  XTH ), were up-regulated in carpopodium abscission, which reflecting the key roles in regulating the abscission process. The results of transcriptome analysis considerably conformed with those of proteome analysis as documented previously. In comparison with those of the retention fruitlet, the auxin contents in abscising carpopodium were significantly low, which presumably increased the ethylene sensitivity of the abscission zone, conversely, the abscisic acid (ABA) accumulation was considerably higher in abscising carpopodium. Furthermore, the ratio of (TZ + IAA + GA3) / ABA also obviously lower in abscising carpopodium. Besides, the HD-ZIP gene family analysis showed that  PavHB16  and  PavHB18  were up-regulated in abscising organs.    Conclusion  Our findings combine morphology, cytology and transcriptional regulation to reveal the molecular mechanism of sweet cherry fruitlet abscission. It provides a new perspective for further study of plant organ shedding.    Supplementary Information  The online version contains supplementary material available at 10.1186/s12870-021-02940-8.

bmc plant biology

Cross-talk between transcriptome, phytohormone and HD-ZIP gene family analysis illuminates the molecular mechanism underlying fruitlet abscission in sweet cherry (Prunus avium L)