HUA ENHANCER1 Mediates Ovule Development

Abstract

Ovules are female reproductive organs of angiosperms, containing sporophytic integuments and gametophytic embryo sacs. After fertilization, embryo sacs develop into embryos and endosperm whereas integuments into seed coat. Ovule development is regulated by transcription factors (TF) whose expression is often controlled by microRNAs. Mutations of Arabidopsis DICER-LIKE 1 (DCL1), a microRNA processing protein, caused defective ovule development and reduced female fertility. However, it was not clear whether other microRNA processing proteins participate in this process and how defective ovule development influenced female fertility. We report that mutations of HUA ENHANCER1 (HEN1) and HYPONASTIC LEAVES 1 (HYL1) interfered with integument growth. The sporophytic defect caused abnormal embryo sac development and inability of mutant ovules to attract pollen tubes, leading to reduced female fertility. We show that the role of HEN1 in integument growth is cell-autonomous. Although AUXIN RESPONSE FACTOR 6 (ARF6) and ARF8 were ectopically expressed in mutant ovules, consistent with the reduction of microRNA167 in hen1, introducing arf6;arf8 did not suppress ovule defects of hen1, suggesting the involvement of more microRNAs in this process. Results presented indicate that the microRNA processing machinery is critical for ovule development and seed production through multiple microRNAs and their targets.

Big Role of Small RNAs in Female Gametophyte Development

“…Besides, the defects of ovule development in the mir167 mutant can be rescued by introducing either arf6 or arf8 [35]. Furthermore, a significant reduction in the accumulation of miR167 is observed in hen1 mutants resulting in ectopic expression of ARF6 and ARF8 and introduction of arf6; arf8 failed to rescue the ovule defects in hen1 mutant [36][37][38]. Consistently, miR165/6 targets Class III HOMEODOMAIN-LEUCINE ZIPPER (HD-Zip III) gene PHABULOSA (PHB) [39].…”

The emerging role of small RNAs in ovule development, a kind of magic

“…In fact, the corresponding mutants present defects in inner and outer integuments development. Gametogenesis is impaired in an ARGONAUTE 5 (AGO5) mutant, showing a high percentage of ovule abortion; the predicted AGO5 protein shares a similar protein structure with some viral suppressor proteins, e.g., P1/Hc-Pro and P19, that are known to inhibit miRNA and siRNA functions Recently, two other miRNA-processing proteins HUA1 and HYL1 have been reported to be required for normal integument growth (Wei et al 2020). HYL1, a dsRNAbinding protein, interacts with DCL1 during the processing of pri-miRNAs (Kurihara et al 2006), while HEN1 is a O-methyltransferase critical for miRNA biogenesis (Baranauske et al 2015).…”

“…Recently, two other miRNA-processing proteins HUA1 and HYL1 have been reported to be required for normal integument growth (Wei et al 2020 ). HYL1, a dsRNA-binding protein, interacts with DCL1 during the processing of pri-miRNAs (Kurihara et al 2006 ), while HEN1 is a O-methyltransferase critical for miRNA biogenesis (Baranauske et al 2015 ).…”

“…In plants with no HEN1 activity, small RNAs accumulate at a lower level and present heterogeneous size (Yu et al 2005 ). hen1-8 and hyl1-2 ovules failed to grow asymmetric integuments, leading to defective embryo sac development; thus, it compromises pollen tube guidance, causing reduced fertility (Wei et al 2020 ). Ectopic expression of ARF6 and ARF8 in hen1-8 ovules was consistent with the reduction of miRNA167 , whose processing relies on HEN1 (Yu et al 2010 ).…”

Emerging Roles of RNA-Binding Proteins in Seed Development and Performance

“…Mutations in miRNA processing genes also affect embryo formation and development. The mutant of DCL1 short integuments ( sin1 / dcl1-7 ), the hypomorphic mutant of HEN1 ( hen1-8 ), and the null mutant of HYL1 ( hyl1-2 ) are defective in asymmetric growth of the integuments, leading to abnormal ovule development and reduced female fertility [ 79 , 80 ]. Embryo patterning from the zygote to the globular stage is also severely affected in the dcl1 and hyl1-2 mutants.…”