Snow alga Sanguina aurantia as revealed through de novo genome assembly and annotation.

To thrive on melting alpine and polar snow, some Chlorophytes produce an abundance of astaxanthin, causing red blooms, often dominated by genus Sanguina. The red cells have not been cultured, but we recently grew a green biciliate conspecific with Sanguina aurantia from a sample of watermelon snow. This culture provided source material for Oxford Nanopore Technology and Illumina sequencing.

Rosetta gen. nov. (Chlorophyta): Resolving the identity of red snow algal rosettes.

Thick-walled rosette-like snow algae were long thought to be a life stage of various other species of snow algae. Rosette-like cells have not been cultured, but by manually isolating cells from 38 field samples in southern British Columbia, we assigned a variety of rosette morphologies to DNA sequence. Phylogenetic analysis of Rubisco large-subunit (rbcL) gene, ribosomal internal transcribed spacer 2 (ITS2) rRNA region, and 18S rRNA gene revealed that the rosette-like cells form a new clade within the phylogroup Chloromonadinia.

Satellite mapping of red snow on North American glaciers.

Red snow caused by blooms of microalgae darkens the surface of summer snowfields, increasing snowmelt. To assess the contribution of red snow to supraglacial snowmelt in northwestern North America, we systematically mapped the 2019-2022 distribution of blooms by applying supervised classification to 6158 satellite images. Blooms occurred on 5% of the total glaciated area, heavily affecting many glaciers in years of prolonged snow cover duration.

A metagenomic study of the bacteria in snow algae microbiomes.

The bacterial communities found in snow algae blooms have been described in terms of their 16S rRNA gene community profiles, but little information exists on their metabolic potential. Previously, we reported that several bacterial taxa are common across snow algae blooms in the southwestern mountains of the Coast Range in British Columbia, Canada. Here, we further this work by reporting a partial bacterial metagenome from the same snow algal microbiomes.

The underlying green biciliate morphology of the orange snow alga Sanguina aurantia.

In the summer, blooms of microalgae appear on alpine and polar snowfields, creating expanses of red snow sometimes called 'watermelon snow'. These blooms are attracting research attention because they decrease snow albedo, thereby accelerating the effects of global warming on snowmelt. Currently, meltwater from alpine snowfields provides one-sixth of the world's population with water for drinking, agriculture, and the generation of hydroelectric power.

A Molecular Analysis of Microalgae from Around the Globe to Revise Raphidonema (Trebouxiophyceae, Chlorophyta).

We isolated five microalgal strains from alpine snow near Vancouver, Canada, which display morphological features suggestive of the genera Koliella and Raphidonema. Due to variations in cell size and shape, we could not make a clear delimitation based on morphology. We proceeded to a molecular analysis and included 22 strains from the CCCryo culture collection, previously identified as members of four closely related genera: Raphidonema, Koliella, Stichococcus, and Pseudochlorella.

Alpine Snow Algae Microbiome Diversity in the Coast Range of British Columbia.

Snow algae blooms contain bacteria, fungi, and other microscopic organisms. We surveyed 55 alpine snow algae blooms, collecting a total of 68 samples, from 12 mountains in the Coast Range of British Columbia, Canada. We used microscopy and rDNA metabarcoding to document biodiversity and query species and taxonomic associations.

Variation in Snow Algae Blooms in the Coast Range of British Columbia.

Snow algae blooms cover vast areas of summer snowfields worldwide, reducing albedo and increasing snow melt. Despite their global prevalence, little is known about the algae species that comprise these blooms. We used 18S and metabarcoding and light microscopy to characterize algae species composition in 31 snow algae blooms in the Coast Range of British Columbia, Canada.

Cilia in cystic kidney and other diseases.

Epithelial cells lining the ducts and tubules of the kidney nephron and collecting duct have a single non-motile cilium projecting from their surface into the lumen of the tubule. These organelles were long considered vestigial remnants left as a result of evolution from a ciliated ancestor, but we now recognize them as critical sensory antennae. In the kidney, the polycystins and fibrocystin, products of the major human polycystic kidney disease genes, localize to this organelle.

A Forward Genetic Screen and Whole Genome Sequencing Identify Deflagellation Defective Mutants in Chlamydomonas, Including Assignment of ADF1 as a TRP Channel.

With rare exception, ciliated cells entering mitosis lose their cilia, thereby freeing basal bodies to serve as centrosomes in the formation of high-fidelity mitotic spindles. Cilia can be lost by shedding or disassembly, but either way, it appears that the final release may be via a coordinated severing of the nine axonemal outer doublet microtubules linking the basal body to the ciliary transition zone. Little is known about the mechanism or regulation of this important process.

Cilia assembly: a role for F-actin in IFT recruitment.

Ciliary growth rates are limited by the availability of precursors at the growing tip. A new paper reveals that the early rapid growth of nascent cilia is supported by F-actin-facilitated delivery of IFT proteins to basal bodies.

The kinases LF4 and CNK2 control ciliary length by feedback regulation of assembly and disassembly rates.

Background: Many of the diverse functions of cilia depend upon tight control of their length. Steady-state length reflects a balance between rates of ciliary assembly and disassembly, two parameters likely controlled by a length sensor of unknown identity or mechanism.

Results: A null mutation in Chlamydomonas CNK2, a member of the evolutionarily conserved family of NIMA-related kinases, reveals feedback regulation of assembly and disassembly rates.

Centrioles are freed from cilia by severing prior to mitosis.

Cilia are necessary for normal tissue development and homeostasis and are generally present during interphase, but not in mitosis. The precise mechanism of premitotic ciliary loss has been controversial, with data supporting either sequential disassembly through the transition zone or, alternatively, a severing event at the base of the cilia. Here we show by live cell imaging and immunofluorescence microscopy that resorbing flagella of Chlamydomonas leave remnants associated with the mother cell wall.

Individuals with mutations in XPNPEP3, which encodes a mitochondrial protein, develop a nephronophthisis-like nephropathy.

The autosomal recessive kidney disease nephronophthisis (NPHP) constitutes the most frequent genetic cause of terminal renal failure in the first 3 decades of life. Ten causative genes (NPHP1-NPHP9 and NPHP11), whose products localize to the primary cilia-centrosome complex, support the unifying concept that cystic kidney diseases are "ciliopathies". Using genome-wide homozygosity mapping, we report here what we believe to be a new locus (NPHP-like 1 [NPHPL1]) for an NPHP-like nephropathy.

Sensorium: the original raison d'etre of the motile cilium?

The role of non-motile (primary) cilia as sensory antennae critical for metazoan development and physiology has surfaced over the last decade, long after the function of motile cilia in propelling cells or moving fluids across tissues was well established. A new study of motile cilia from respiratory airways raises the possibility that transducing sensory cues from the environment is a universal characteristic of cilia and may have been the original raison d'être of the ancestral cilium.

The NIMA-related kinase NEK1 cycles through the nucleus.

Mutations in NEK1 in mice are causal for cystic kidneys, and model the ciliopathy polycystic kidney disease caused by abnormal ciliary structure or signaling. NEK1 has previously been shown to localize near centrosomes and to play a role in centrosomal stability and ciliogenesis. Recent data suggest that the etiology of kidney cysts involves aberrant signaling from the primary cilium to the nucleus.

Ciliary ion channels: location, location, location.

The elegant waveforms of motile cilia derive from temporal and spatial regulation of dynein-driven microtubule sliding. A new study reveals the surprising localization of the channel responsible for waveform switch.

Functional interactions between the ciliopathy-associated Meckel syndrome 1 (MKS1) protein and two novel MKS1-related (MKSR) proteins.

Meckel syndrome (MKS) is a ciliopathy characterized by encephalocele, cystic renal disease, liver fibrosis and polydactyly. An identifying feature of MKS1, one of six MKS-associated proteins, is the presence of a B9 domain of unknown function. Using phylogenetic analyses, we show that this domain occurs exclusively within a family of three proteins distributed widely in ciliated organisms.

Katanin knockdown supports a role for microtubule severing in release of basal bodies before mitosis in Chlamydomonas.

Katanin is a microtubule-severing protein that participates in the regulation of cell cycle progression and in ciliary disassembly, but its precise role is not known for either activity. Our data suggest that in Chlamydomonas, katanin severs doublet microtubules at the proximal end of the flagellar transition zone, allowing disengagement of the basal body from the flagellum before mitosis. Using an RNA interference approach we have discovered that severe knockdown of the p60 subunit of katanin, KAT1, is achieved only in cells that also carry secondary mutations that disrupt ciliogenesis.

The NIMA-family kinase, Nek1 affects the stability of centrosomes and ciliogenesis.

Background: Mutations in Nek1 (NIMA-Related Kinase 1) are causal in the murine models of polycystic kidney disease kat and kat2J. The Neks are known as cell cycle kinases, but recent work in protists has revealed that in addition to roles in the regulation of cell cycle progression, some Neks also regulate cilia. In most cells, cilia are disassembled prior to mitosis and are regenerated after cytokinesis.

NEK8 mutations affect ciliary and centrosomal localization and may cause nephronophthisis.

Nephronophthisis, an autosomal recessive kidney disease, is the most frequent genetic cause of chronic renal failure in the first 3 decades of life. Causative mutations in 8 genes (NPHP1-8) have been identified, and homologous mouse models for NPHP2/INVS and NPHP3 have been described. The jck mouse is another model of recessive cystic kidney disease, and this mouse harbors a missense mutation, G448V, in the highly conserved RCC1 domain of Nek8.

Defects in ciliary localization of Nek8 is associated with cystogenesis.

Mutations in the human NIMA (Never in Mitosis gene A)-related kinase 8 (Nek8) are associated with a rare form of the juvenile renal cystic disease, nephronophthisis type 9, and mutations in murine Nek8 cause renal cysts in jck mice. Cystogenesis involves dysfunctional ciliary signaling, and we have previously reported that Nek8 localizes to the primary cilium in mouse kidney epithelial cells. We now report that in developing mouse kidney, Nek8 is detected in the cilia of a subset of ureteric-bud-derived tubules at embryonic day (E)15.