Faithful chromosome segregation is required for both mitotic and meiotic cell divisions and is regulated by multiple mechanisms including the anaphase‐promoting complex/cyclosome ( We used a combination of genetic analyses, cytology and immunolocalisation to define the function of At Meiocytes from Our results demonstrate that Arabidopsis
Haspin‐mediated phosphorylation of histone H3 at threonine 3 (H3T3ph) promotes proper deposition of Aurora B at the inner centromere to ensure faithful chromosome segregation in metazoans. However, the function of H3T3ph remains relatively unexplored in plants. Here, we show that in maize (
- PAR ID:
- 10046419
- Publisher / Repository:
- Wiley-Blackwell
- Date Published:
- Journal Name:
- The Plant Journal
- Volume:
- 92
- Issue:
- 6
- ISSN:
- 0960-7412
- Page Range / eLocation ID:
- p. 1121-1131
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
More Like this
-
Summary APC /C), which is the largest known E3 ubiquitin‐ligase complex and has been implicated in regulating chromosome segregation in both mitosis and meiosis in animals. However, the role of theAPC /C during plant meiosis remains largely unknown. Here, we show that Arabidopsis is required for male meiosis.APC 8APC 8 in male meiosis.apc8‐1 plants exhibit several meiotic defects including improper alignment of bivalents at metaphase I, unequal chromosome segregation during anaphaseII , and subsequent formation of polyads. Immunolocalisation using an antitubulin antibody showed thatAPC 8 is required for normal spindle morphology. We also observed mitotic defects inapc8‐1, including abnormal sister chromatid segregation and microtubule morphology.APC /C is required for meiotic chromosome segregation and thatAPC /C‐mediated regulation of meiotic chromosome segregation is a conserved mechanism among eukaryotes. -
null (Ed.)Abstract Centromeres are epigenetically determined nuclear domains strictly required for chromosome segregation and genome stability. However, the mechanisms regulating centromere and kinetochore chromatin modifications are not known. Here, we demonstrate that LSH is enriched at meiotic kinetochores and its targeted deletion induces centromere instability and abnormal chromosome segregation. Superresolution chromatin analysis resolves LSH at the inner centromere and kinetochores during oocyte meiosis. LSH knockout pachytene oocytes exhibit reduced HDAC2 and DNMT-1. Notably, mutant oocytes show a striking increase in histone H3 phosphorylation at threonine 3 (H3T3ph) and accumulation of major satellite transcripts in both prophase-I and metaphase-I chromosomes. Moreover, knockout oocytes exhibit centromere fusions, ectopic kinetochore formation and abnormal exchange of chromatin fibers between paired bivalents and asynapsed chromosomes. Our results indicate that loss of LSH affects the levels and chromosomal localization of H3T3ph and provide evidence that, by maintaining transcriptionally repressive heterochromatin, LSH may be essential to prevent deleterious meiotic recombination events at repetitive centromeric sequences.more » « less
-
De novo centromere formation on chromosome fragments with an inactive centromere in maize (Zea mays)
Abstract The B chromosome of maize undergoes nondisjunction at the second pollen mitosis as part of its accumulation mechanism. Previous work identified 9-Bic-1 (9-B inactivated centromere-1), which comprises an epigenetically silenced B chromosome centromere that was translocated to the short arm of chromosome 9(9S). This chromosome is stable in isolation, but when normal B chromosomes are added to the genotype, it will attempt to undergo nondisjunction during the second pollen mitosis and usually fractures the chromosome in 9S. These broken chromosomes allow a test of whether the inactive centromere is reactivated or whether a de novo centromere is formed elsewhere on the chromosome to allow recovery of fragments. Breakpoint determination on the B chromosome and chromosome 9 showed that mini chromosome B1104 has the same breakpoint as 9-Bic-1 in the B centromere region and includes a portion of 9S. CENH3 binding was found on the B centromere region and on 9S, suggesting both centromere reactivation and de novo centromere formation. Another mini chromosome, B496, showed evidence of rearrangement, but it also only showed evidence for a de novo centromere. Other mini chromosome fragments recovered were directly derived from the B chromosome with breakpoints concentrated near the centromeric knob region, which suggests that the B chromosome is broken at a low frequency due to the failure of the sister chromatids to separate at the second pollen mitosis. Our results indicate that both reactivation and de novo centromere formation could occur on fragments derived from the progenitor possessing an inactive centromere.
-
Summary Many
Actinidia cultivars are characterized by anthocyanin accumulation, specifically in the inner pericarp, but the underlying regulatory mechanism remains elusive. Here we report two interacting transcription factors, AcMYB 123 and AcbHLH 42, that regulate tissue‐specific anthocyanin biosynthesis in the inner pericarp ofActinidia chinensis cv. Hongyang. Through transcriptome profiling analysis we identified fiveMYB and threebHLH transcription factors that were upregulated in the inner pericarp. We show that the combinatorial action of two of them, AcMYB 123 and AcbHLH 42, is required for activating promoters ofAcANS andAcF3GT1 that encode the dedicated enzymes for anthocyanin biosynthesis. The presence of anthocyanin in the inner pericarp appears to be tightly associated with elevated expression ofAcMYB123 andAcbHLH42 .RNA interference repression ofAcMYB123 ,AcbHLH42 ,AcF3GT1 andAcANS in ‘Hongyang’ fruits resulted in significantly reduced anthocyanin biosynthesis. Using both transient assays inNicotiana tabacum leaves orActinidia arguta fruits and stable transformation in Arabidopsis, we demonstrate that co‐expression ofAcMYB123 andAcbHLH42 is a prerequisite for anthocyanin production by activating transcription ofAcF3GT1 andAcANS or the homologous genes. Phylogenetic analysis suggests that AcMYB 123 or AcbHLH 42 are closely related toTT 2 orTT 8, respectively, which determines proanthocyanidin biosynthesis in Arabidopsis, and to anthocyanin regulators in monocots rather than regulators in dicots. All these experimental results suggest that AcMYB 123 and AcbHLH 42 are the components involved in spatiotemporal regulation of anthocyanin biosynthesis specifically in the inner pericarp of kiwifruit. -
Summary Boron is a micronutrient that is required for the normal growth and development of vascular plants, but its precise functions remain a subject of debate. One established role for boron is in the cell wall where it forms a diester cross‐link between two monomers of the low‐abundance pectic polysaccharide rhamnogalacturonan‐
II (RG ‐II ). The inability ofRG ‐II to properly assemble into a dimer results in the formation of cell walls with abnormal biochemical and biomechanical properties and has a severe impact on plant productivity. Here we describe the effects onRG ‐II structure and cross‐linking and on the growth of plants in which the expression of aGDP ‐sugar transporter (GONST 3/GGLT 1) has been reduced. In the ‐silenced plants the amount of L‐galactose in side‐chain A ofGGLT 1RG ‐II is reduced by up to 50%. This leads to a reduction in the extent ofRG ‐II cross‐linking in the cell walls as well as a reduction in the stability of the dimer in the presence of calcium chelators. The silenced plants have a dwarf phenotype, which is rescued by growth in the presence of increased amounts of boric acid. Similar to themur1 mutant, which also disruptsRG ‐II cross‐linking, ‐silenced plants display a loss of cell wall integrity under salt stress. We conclude thatGGLT 1GGLT 1 is probably the primary GolgiGDP ‐L‐galactose transporter, and providesGDP ‐L‐galactose forRG ‐II biosynthesis. We propose that the L‐galactose residue is critical forRG ‐II dimerization and for the stability of the borate cross‐link.