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Velasquez, S. M.

Publications and source records attributed to Velasquez, S. M..

5 recordsLinked to original sources

Evidence for an ancient master sex determination gene in Hymenoptera

The vast majority of Hymenopterans determine sex by haplodiploidy, in which males and females develop from haploid unfertilized and diploid fertilized eggs, respectively. At the molecular level, the majority of Hymenoptera are thought to determine sex by so-called Complementary Sex Determination (CSD). Under CSD, sex is determined by the feminizing effects of one or more allele-rich loci, in which the feminizing function is imparted by the interactions of functionally distinct alleles. Because of high allelic diversity, most diploids are heterozygous and develop as females, whereas haploid individuals develop as males, as do rare homozygous diploids. Despite diverse empirical results suggesting that CSD is widespread in Hymenopterans, and substantial theoretical and empirical study of the consequences of CSD, the molecular biology of CSD has received little attention outside of the honeybee, Apis mellifera. Available evidence provides support for divergent perspectives ranging from a single (nearly) universally-conserved CSD locus or a pattern dominated by evolutionary turnover with different genes serving as the CSD gene(s) in different lineages. Recently, a novel non-coding RNA gene named ANTSR was shown to serve as a CSD gene in different ant lineages, and the authors suggested that ANTSR might serve as a more broadly-conserved CSD gene. To assess the role of ANTSR role in CSD across diverse Hymenoptera, we studied syntenic conservation and polymorphism patterns in the broad ANTSR locus, genome-wide sequence from available male and female diploid Formica ants, and data from a sibling cross for Bombus terrestris. We find evidence that ANTSR is a conserved CSD gene across diverse Aculeata, the largest group of Hymenoptera, and provide preliminary evidence that Formica may have multiple CSD loci including ANTSR.

genetics↗

Proline-rich Extensin-like Receptor Kinases PERK5 and PERK12 are involved in Pollen Tube Growth

BackgroundCell wall integrity plays an essential role during polarized cell growth typical of pollen tubes and root hairs. Proline-rich Extensin-like Receptor Kinases (PERK) belong to the hydroxyproline-rich glycoprotein (HRGP) superfamily of cell surface glycoproteins. ResultsHere, we identified two PERKs from Arabidopsis thaliana, PERK5 and PERK12 highly expressed in mature pollen. Pollen tube growth was impaired in the single and double perk5-1 perk12-1 loss of function mutants, with a moderate impact on seed production. When the segregation of self- and reciprocal-crosses of the perk5-1, perk5-2 and perk12-1 single mutants, and reciprocal-crosses of the perk5-1 perk12-1 double mutant were carried out, a male gametophytic defect was found, indicating that perk5-1 and perk12-1 mutants carry defective pollen tubes, resulting in deficient pollen transmission. Furthermore, double perk5-1 perk12-1 mutants show excessive accumulation of pectins and cellulose at the cell wall pollen of the tube tip. In addition, an upregulation of cytoplasmic ROS levels were detected by using 2,7-dichlorofluorescein diacetate probe (H2DCF-DA), and in agreement, similar results were obtained with HyPer, a genetically encoded YFP-based radiometric sensor, which is used to follow the production of hydrogen peroxide (H2O2). Single and double perk5-1 perk12-1 mutants show higher levels of cytoplasmic H2O2 in their pollen tube tips. ConclusionsTaken together, our results suggest that PERK5 and PERK12 are necessary for proper pollen tube growth highlighting their role on cell wall assembly and ROS homeostasis.

plant biology↗

Auxin-dependent xyloglucan remodelling defines differential tissue expansion in Arabidopsis thaliana

Size control is a fundamental question in biology, showing incremental complexity in case of plants whose cells possess a rigid cell wall. The phytohormone auxin is a vital growth regulator with central importance for differential growth control. Here we show that growth inducing and repressing auxin conditions correlate with reduced and enhanced complexity of extracellular xyloglucans, respectively. In agreement, genetic interference with xyloglucan complexity distinctly modulates auxin-dependent differential growth rates. Our work proposes that an auxin-dependent, spatially defined effect on xyloglucan structure and its effect on cell wall mechanics specify differential, gravitropic hypocotyl growth.

plant biology↗

A cell surface O-glycosylated peptide, AGP21, acts on the brassinosteroid pathway and modulates root hair cell fate

Root hairs (RHs) develop from specialized epidermal cells called trichoblasts, whereas epidermal cells that lack RHs are known as atrichoblasts. The mechanism controlling root epidermal cell fate is only partially understood. Root epidermis cell fate is regulated by a transcription factor complex that promotes the expression of the homeodomain protein GLABRA 2 (GL2), which blocks RH development by inhibiting ROOT HAIR DEFECTIVE 6 (RHD6). Suppression of GL2 expression activates RHD6, a series of downstream TFs including ROOT HAIR DEFECTIVE 6 LIKE-4 (RSL4 [Yi et al. 2010]) and their target genes, and causes epidermal cells to develop into RHs. Brassinosteroids (BRs) influence root epidermis cell fate. In the absence of BRs, phosphorylated BIN2 (a Type-II GSK3-like kinase) inhibits a protein complex that directly downregulates GL2 [Chen et al. 2014]. Here, we show that the genetic and pharmacological perturbation of the arabinogalactan peptide (AG) AGP21 in Arabidopsis thaliana, triggers aberrant RH development, similar to that observed in plants with defective BR signaling. We reveal that an O-glycosylated AGP21 peptide, which is positively regulated by BZR1, a transcription factor activated by BR signaling, affects RH cell fate by altering GL2 expression in a BIN2-dependent manner. These results suggest that perturbation of a cell surface AGP disrupts BR responses and inhibits the downstream effect of BIN2 on the RH repressor GL2 in root epidermal cells. In addition, AGP21 also acts in a BR-independent, AGP-dependent mode that together with BIN2 signalling cascade controls RH cell fate. SignificanceIn the plant Arabidopsis thaliana, the root epidermis forms in an alternating pattern atrichoblasts with trichoblast cells that end up developing root hairs (RHs). Atrichoblast cell fate is directly promoted by the transcription factor GLABRA2 (GL2) while the lack of GL2 allows RH formation. The loss of AGP21 peptide triggers an abnormal RH cell fate in two contiguous cells in a similar manner as brassinosteroid (BRs) mutants. In the absence of BR signaling, BIN2 (a GSK3 like-kinase) in a phosphorylated state, downregulate GL2 expression to trigger RH cell fate. The absence of AGP21 is able to repress GL2 expression and activates the expression of RSL4 and EXP7 root hair proteins.

plant biology↗

The Molecular Link Between Auxin And ROS-Mediated Polar Growth

Root hair polar growth is endogenously controlled by auxin and sustained by oscillating levels of reactive oxygen species (ROS). These cells extend several hundred-fold their original size toward signals important for plant survival. Although their final cell size is of fundamental importance, the molecular mechanisms that control it remain largely unknown. Here, we show that ROS production is controlled by the transcription factors RSL4, which in turn is transcriptionally regulated by auxin through several Auxin Responsive Factors (ARFs). In this manner, auxin controls ROS-mediated polar growth by activating RSL4, which then upregulates the expression of genes encoding NADPH oxidases (also known as RBOHs, RESPIRATORY BURST OXIDASE HOMOLOG proteins) and Class-III Peroxidases (PER), which catalyse ROS production. Chemical or genetic interference with the ROS balance or peroxidase activity affect root hair final cell size. Overall, our findings establish a molecular link between auxin regulated ARFs-RSL4 and ROS-mediated polar root hair growth.\n\nSignificance StatementTip-growing root hairs are excellent model systems to decipher the molecular mechanism underlying reactive oxygen species (ROS)-mediated cell elongation. Root hairs are able to expand in response to external signals, increasing several hundred-fold their original size, which is important for survival of the plant. Although their final cell size is of fundamental importance, the molecular mechanisms that control it remain largely unknown. In this study, we propose a molecular mechanism that links the auxin-Auxin Response Factors (ARFs) module to activation of RSL4, which directly targets genes encoding ROS-producing enzymes, such as NADPH oxidases (or RBOHs) and secreted type-III peroxidases (PERs). Activation of these genes impacts apoplastic ROS homeostasis, thereby stimulating root hair cell elongation.

plant biology↗