Chlamydomonas reinhardtii is a unicellular green alga whose lineage diverged from land plants over 1 billion years ago. It is a model system for studying chloroplast-based photosynthesis, as well as the structure, assembly, and function of eukaryotic flagella (cilia), which were inherited from the common ancestor of plants and animals, but lost in land plants. We sequenced the~120-megabase nuclear genome of Chlamydomonas and performed comparative phylogenomic analyses, identifying genes encoding uncharacterized proteins that are likely associated with the function and biogenesis of chloroplasts or eukaryotic flagella. Analyses of the Chlamydomonas genome advance our understanding of the ancestral eukaryotic cell, reveal previously unknown genes associated with photosynthetic and flagellar functions, and establish links between ciliopathy and the composition and function of flagella.

The steroid dexamethasone improves survival in severe cases of COVID-19.

No abstract

Disease resistance in Arabidopsis is regulated by multiple signal transduction pathways in which salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) function as key signaling molecules. Epistasis analyses were performed between mutants that disrupt these pathways (npr1, eds5, ein2, and jar1) and mutants that constitutively activate these pathways (cpr1, cpr5, and cpr6), allowing exploration of the relationship between the SA- and JA/ET-mediated resistance responses. Two important findings were made. First, the constitutive disease resistance exhibited by cpr1, cpr5, and cpr6 is completely suppressed by the SA-deficient eds5 mutant but is only partially affected by the SA-insensitive npr1 mutant. Moreover, eds5 suppresses the SA-accumulating phenotype of the cpr mutants, whereas npr1 enhances it. These data indicate the existence of an SA-mediated, NPR1-independent resistance response. Second, the ET-insensitive mutation ein2 and the JA-insensitive mutation jar1 suppress the NPR1-independent resistance response exhibited by cpr5 and cpr6. Furthermore, ein2 potentiates SA accumulation in cpr5 and cpr5 npr1 while dampening SA accumulation in cpr6 and cpr6 npr1. These latter results indicate that cpr5 and cpr6 regulate resistance through distinct pathways and that SA-mediated, NPR1-independent resistance works in combination with components of the JA/ET-mediated response pathways.

Barely a week has elapsed since scientists in Botswana and South Africa alerted the world to a fast-spreading SARS-CoV-2 variant now known as Omicron. Researchers worldwide are racing to understand the threat that the variant -now confirmed in more than 30 countries -poses to the world. Yet it might take scientists weeks to paint a more complete picture of Omicron, and to gain an understanding of its transmissibility and severity, as well as its potential to evade vaccines and cause reinfections."There is so little understanding of what's going on, and that's true even for scientists," says Senjuti Saha, a molecular microbiologist and director of the Child Health Research Foundation in Dhaka, Bangladesh.Nature rounds up what scientists know so far about the Omicron variant.

No abstract

Disease resistance in Arabidopsis is regulated by multiple signal transduction pathways in which salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) function as key signaling molecules. Epistasis analyses were performed between mutants that disrupt these pathways ( npr1 , eds5 , ein2 , and jar1 ) and mutants that constitutively activate these pathways ( cpr1, cpr5 , and cpr6 ), allowing exploration of the relationship between the SA-and JA/ET-mediated resistance responses. Two important findings were made. First, the constitutive disease resistance exhibited by cpr1 , cpr5, and cpr6 is completely suppressed by the SA-deficient eds5 mutant but is only partially affected by the SA-insensitive npr1 mutant. Moreover, eds5 suppresses the SA-accumulating phenotype of the cpr mutants, whereas npr1 enhances it. These data indicate the existence of an SA-mediated, NPR1-independent resistance response. Second, the ET-insensitive mutation ein2 and the JA-insensitive mutation jar1 suppress the NPR1-independent resistance response exhibited by cpr5 and cpr6 . Furthermore, ein2 potentiates SA accumulation in cpr5 and cpr5 npr1 while dampening SA accumulation in cpr6 and cpr6 npr1 . These latter results indicate that cpr5 and cpr6 regulate resistance through distinct pathways and that SA-mediated, NPR1-independent resistance works in combination with components of the JA/ETmediated response pathways. INTRODUCTIONIn plants, resistance to pathogen infection is accomplished through protective physical barriers and a diverse array of antimicrobial chemicals and proteins. Many of these antimicrobial compounds are part of an active defense response, and their rapid induction is contingent on the plant's ability to recognize and respond to an invading pathogen (Staskawicz et al., 1995;Baker et al., 1997). Pathogen recognition often involves the interaction of an avirulence signal (encoded by pathogen avr genes) and cognate plant resistance gene (R) products (Staskawicz et al., 1995;Bent, 1996;Baker et al., 1997). The avr/R interaction often triggers a strong defense mechanism known as the hypersensitive response (HR) (Flor, 1947(Flor, , 1971 Keen, 1990;Van Der Biezen and Jones, 1998). In general, pathogens that activate avr/Rmediated signaling pathways do not cause disease and are said to be avirulent.An HR activated by avr/R signaling is characterized by several physiological changes, including the accumulation of reactive oxygen intermediates, nitric oxide, and salicylic acid (SA) (Dangl et al., 1996; Hammond-Kosack and Jones, 1996; Low and Merida, 1996;Lamb and Dixon, 1997; Delledonne et al., 1998; Durner et al., 1998). Jasmonic acid (JA) and ethylene (ET) are also produced in response to pathogen infection, most probably because of an increase in lipoxygenase and 1-amino-cyclopropane-1-carboxylic acid (ACC) oxidase activities, respectively (Gundlach et al., 1992; HammondKosack et al., 1996; May et al., 1996; Penninckx et al., 1996;Thomma et al., 1998). SA, JA, and ET induce the production of antimicrobial compounds such...

Photosynthetic organisms constantly face the threat of photo-oxidative stress from fluctuating light conditions and environmental stress. Plants and algae have developed an array of defences to protect the chloroplast from reactive oxygen species. Genetic and physiological studies have shown that antioxidant responses are important to highlight acclimation, both by directly scavenging or quenching reactive oxygen intermediates and by contributing reducing power for alternative electron transport pathways and excess energy dissipation. At present, the signalling events leading to up-regulation of antioxidant defences in high light remain a mystery. Recent advances toward understanding acclimation to oxidative stress in both photosynthetic and non-photosynthetic model organisms may illuminate how plants and algae respond to high-light stress. Although the role of hydrogen peroxide in highlight acclimation has been investigated, less is known about responses to singlet oxygen, a form of reactive oxygen that poses a significant threat specifically to photosynthetic organisms. This review will discuss some intriguing new findings in that area, focusing on recent findings regarding the nature of singlet-oxygen responses in the chloroplast.