The Chlamydomonas mex1 mutant shows impaired starch mobilization without maltose accumulation

Abstract

The MEX1 locus of Chlamydomonas reinhardtii was identified in a genetic screen as a factor that affects starch metabolism. Mutation of MEX1 causes a slow-down in the mobilization of storage polysaccharide. Cosegregation and functional complementation analyses were used to assess the involvement of the Mex1 protein in starch degradation. Heterologous expression experiments performed in Escherichia coli and Arabidopsis thaliana allowed us to test the capacity of the algal protein in maltose export. In contrast to the A. thaliana mex1 mutant, the mutation in C. reinhardtii does not lead to maltose accumulation and growth impairment. Although localized in the plastid envelope, the algal protein does not transport maltose efficiently across the envelope, but partly complements the higher plant mutant. Both Mex orthologs restore the growth of the E. coli ptsG mutant strain on glucose-containing medium, revealing the capacity of these proteins to transport this hexose. These findings suggest that Mex1 is essential for starch mobilization in both Chlamydomonas and Arabidopsis, and that this protein family may support several functions and not only be restricted to maltose export across the plastidial envelope.

A Chloroplast COR413 Protein From Physcomitrella patens Is Required for Growth Regulation Under High Light and ABA Responses

“…In plants, the intracellular and intercellular distribution of sugars depends on specific sugar transporters that reside in the plasma membrane or in membranes of different organelles (Bush, 1999;Chen et al, 2015;Hedrich et al, 2015;Patzke et al, 2019). A number of sugar transporters have been identified in chloroplasts, including the maltose exporter MEX1 (Niittylä et al, 2004;Findinier et al, 2017), the plastidic glucose transporter pGlcT (Weber et al, 2000) and the plastidic sugar transporter (pSuT) (Patzke et al, 2019). The analysis of KO mutants altered in sugar transporter genes has highlighted the importance of these genes in developmental and stress responses in plants.…”

The Plastidic Sugar Transporter pSuT Influences Flowering and Affects Cold Responses

“…However, until now, only two plastidic sugar transporters, namely MEX1 and pGlcT, have been characterized at the molecular level. MEX1 exports the starch degradation product maltose (Niittylä et al, 2004;Findinier et al, 2017), and its absence in mutant plants results in the inhibition of starch degradation due to the accumulation of this sugar in the stroma. This metabolic disturbance is connected to growth retardation, which is due to the reduced nocturnal delivery of carbohydrates to the cytosol (Niittylä et al, 2004;Lu and Sharkey, 2006).…”

“…Until now, only two further plastidic sugar transporters, namely MEX1 and pGlcT (Weber et al, 2000;Niittylä et al, 2004), have been identified. Detailed analyses of the physiological properties of mex1 mutants led to the speculation that this carrier might transport, besides maltose, other substrates as well (Ryoo et al, 2013;Findinier et al, 2017). Several plasma membrane-located Suc transporters were shown to transport maltose in addition to Suc (Meyer et al, 2000;Barth et al, 2003;Sivitz et al, 2007); similarly, MEX1 might transport both maltose and Suc.…”

“…However, although the proteinmediated import of sugars into the chloroplast has been known for decades (Wang and Nobel, 1971;Schäfer and Heber, 1977), so far only two plastidic sugar transporters have been identified at the molecular level. These transporters reside in the inner envelope membrane of the chloroplast and either mediate the export of maltose (Maltose Exporter1 [MEX1]; Niittylä et al, 2004;Findinier et al, 2017) or catalyze glucose (Glc) translocation (Plastidic Glc Transporter [pGlcT]; Weber et al, 2000). In mex1 loss-of-function mutants, the defective maltose export results in stromal maltose accumulation that markedly inhibits starch degradation and causes pronounced growth retardation (Niittylä et al, 2004;Lu and Sharkey, 2006), whereas Arabidopsis (Arabidopsis thaliana) mutants lacking pGlcT do not differ substantially from wild-type plants (Cho et al, 2011).…”

Abscisic acid confers salinity tolerance in Chlamydomonas reinhardtii at different stages of its life cycle

“…Green algae are photoautotrophic eukaryotes, which are the ancestors to higher plants (Ligrone, 2019) and, therefore, they are identical to each other in their basic metabolism, including photosynthesis and photoprotection (Delaux et al, 2015). Chlamydomonas reinhardtii is a freshwater unicellular algal model species widely used for studying and revealing many biological aspects of microalgae relevant to higher plants such as evolution (Bell, 2005), biochemistry and physiology (Couso et al, 2018;Girolomoni et al, 2019;Juvale et al, 2016), mutant generation (Findinier et al , 2017;Li et al, 2016;) and algae-based biofuel production (Scranton et al, 2015).Chlamydomonas cells are haploid, and under favorable growth conditions reproduce asexually during the dark phase of the light:dark cycle (Bruce & Bruce, 1981). However, environmental stresses, especially nitrogen limitation, promote sexual reproduction inChlamydomonas , developing plus and minus gametes that mate and fuse to form a zygote, which undergoes meiosis to eventually release four new individual cells (Goodenough et al, 2007).…”