23 Jun 2021
by Mareike Jezek

JXB Volume 72, Issue 13 – Editor’s choice

JXB Volume 72, Issue 13 – Editor’s choice

This article highlights the following publication:

Arabidopsis SMC6A and SMC6B have redundant function in seed and gametophyte development

Wenxuan Zou, Gang Li, Liufang Jian, Jie Qian, Yantong Liu, Jie Zhao

Journal of Experimental Botany, Volume 72, Issue 13, 22 June 2021, Pages 4871–4887, https://doi.org/10.1093/jxb/erab181

JXB Volume 72, Issue 13 – Editor’s choice

Figure 1: Phenotypic characteristics of different AtSMC6A AtSMC6B mutants. (A) Silique phenotype of heterozygous smc6a-/- smc6b+/- mutant containing albino seeds (white arrowheads). (B) Autofluorescence analysis of endosperm development in seeds of wild type (top) and homozygous smc6a-/- smc6b-/- double mutant showing abnormal giant cell nuclei (bottom). (C) Autofluorescence analysis of female gametophyte in wild type seed (top) and seed from smc6b-/- SMC6A-RNAi transgenic plant with abortive embryo sac (bottom).


Mutant albino seeds reveal functions of enigmatic protein complex members in Arabidopsis

Structural integrity of DNA and chromosomes is crucial not only for cell survival but also for the continuity of life. Despite being known for its great physical and chemical stability, DNA is vulnerable to damage especially during critical cell cycle steps such as mitosis and meiosis. DNA protection and repair are facilitated by the so-called Structural Maintenance of Chromosome (SMC) complex that can be found in all eukaryotic cells where it is involved in various DNA-based processes. One of its components is the ring-shaped DNA-binding SMC5/6 complex. Its general structure is relatively conserved yet its functions differ largely among species, making it the most obscure member of the SMC family.

In this issue of JXB Zou et al. focus on the two SMC6 paralogs AtSMC6A and AtSMC6B in Arabidopsis since their function in seed development is yet unclear. The two gene products share high amino acid sequence similarity especially in their conserved domains, they have similar expression patterns, and single knock-out mutants showed no strong phenotype indicating their functional redundancy. Crosses of single smc6a-/- and smc6b-/- mutants did not yield any viable homozygous smc6a-/- smc6b-/- double mutants due to seed abortion, making the further analysis of the genes a real challenge. Fortunately, the authors found white aborted homozygous double mutant seeds in siliques from heterozygous smc6a+/- smc6b-/- and smc6a-/- smc6b+/- plants (Fig. 1A), and these albino seeds served for further comprehensive phenotypic analysis. Tracking the early embryonic development in the seeds showed differences in cell division within the first days after pollination. More embryos remaining in the zygote stage and different types of programmed cell death were observed in the mutant seeds. Furthermore, endosperm cells that surround the embryo contained abnormal giant nuclei (Fig. 1B). These microscopic observations were confirmed through gene expression analysis. Several genes involved in embryo pattern formation were down-regulated in the mutant seeds, whereas positive regulators of programmed cell death were increasingly expressed. Additionally, genes involved in DNA damage response and cell cycle regulation showed altered expression indicating potential roles of AtSMC6A and AtSMC6B in these processes. Lastly, by knocking down AtSMC6A in the smc6b-/- single mutant and AtSMC6B in the smc6a-/- background the authors showed that the two genes are also involved in gametophyte development. Maturity and vitality of pollen grains from these plants was reduced and embryo sac development was impaired (Fig. 1C).

This impressively detailed and comprehensive in-depth study revealed that AtSMC6A and AtSMC6B play important roles in seed and gametophyte development in Arabidopsis. The exact molecular mechanisms underlying the abnormal mutant phenotypes need further exploration. The authors also found different expression levels of AtSMC6A, AtSMC6B and other members of the SMC5/6 complex in AtSOG1 mutants. The transcription factor SOG1 is a central regulator of DNA damage response and these results thus indicate that the SMC5/6 complex may participate in the SOG1-dependent DNA damage repair pathway, a finding that will hopefully be addressed in detail in the future.