Ten-a Affects Fusion of Central Complex Primordia in Drosophila

The central complex of Drosophila melanogaster plays important functions in various behaviors, such as visual and olfactory memory, visual orientation, sleep, and movement control. However little is known about the genes regulating the development of the central complex. Here we report that a mutant gene affecting central complex morphology, cbd (central brain defect), was mapped to ten-a, a type II trans-membrane protein coding gene. Down-regulation of ten-a in pan-neural cells contributed to abnormal morphology of central complex. Over-expression of ten-a by C767-Gal4 was able to partially restore the abnormal central complex morphology in the cbd mutant. Tracking the development of FB primordia revealed that C767-Gal4 labeled interhemispheric junction that separated fan-shaped body precursors at larval stage withdrew to allow the fusion of the precursors. While the C767-Gal4 labeled structure did not withdraw properly and detached from FB primordia, the two fan-shaped body precursors failed to fuse in the cbd mutant. We propose that the withdrawal of C767-Gal4 labeled structure is related to the formation of the fan-shaped body. Our result revealed the function of ten-a in central brain development, and possible cellular mechanism underlying Drosophila fan-shaped body formation

Proposal of optically tunable and reconfigurable multi-channel bandstop filter using sum-frequency generation in a PPLN waveguide

A multi-wavelength bandstop filter is proposed and numerically demonstrated using the sum-frequency generation (SFG) process in a waveguide of periodically poled lithium niobate (PPLN). This proposed device achieves channels number reconfigurable, central filtering wavelength of each filtering channel independently tunable and extinction ratios (ERs) equalized via all-optical methods

<em>Ten-a</em> Affects the Fusion of Central Complex Primordia in <em>Drosophila</em>

<div><p>The central complex of <i>Drosophila melanogaster</i> plays important functions in various behaviors, such as visual and olfactory memory, visual orientation, sleep, and movement control. However little is known about the genes regulating the development of the central complex. Here we report that a mutant gene affecting central complex morphology, <i>cbd</i> (<i>central brain defect</i>), was mapped to <i>ten-a</i>, a type II trans-membrane protein coding gene. Down-regulation of <i>ten-a</i> in pan-neural cells contributed to abnormal morphology of central complex. Over-expression of <i>ten-a</i> by <i>C767</i>-Gal4 was able to partially restore the abnormal central complex morphology in the <i>cbd</i> mutant. Tracking the development of FB primordia revealed that <i>C767</i>-Gal4 labeled interhemispheric junction that separated fan-shaped body precursors at larval stage withdrew to allow the fusion of the precursors. While the <i>C767</i>-Gal4 labeled structure did not withdraw properly and detached from FB primordia, the two fan-shaped body precursors failed to fuse in the <i>cbd</i> mutant. We propose that the withdrawal of <i>C767</i>-Gal4 labeled structure is related to the formation of the fan-shaped body. Our result revealed the function of <i>ten-a</i> in central brain development, and possible cellular mechanism underlying <i>Drosophila</i> fan-shaped body formation.</p> </div

Schematic drawing of genomic region containing <i>ten-a</i>.

<p>(<b>A</b>) Schematic drawing of <i>CG42338</i> (<i>ten-a</i>), <i>CG1924</i>, <i>CG32655</i>, and <i>ten-a</i> deficiency line <i>ten-a^#900</i>. (<b>B</b>) Schematic drawing of mutant site of Ten-a. In <i>cbd ²²⁵⁴</i>, Tryptophan at 1562 is changed to a premature stop codon. In <i>cbd ^KS171</i>, Glycine at 1723 is changed to Serine. In <i>cbd ^KS96</i>, Arginine at 2846 is changed to Cysteine.</p

The expression pattern of <i>C767</i>-Gal4 and DN-cadherin signal during FB formation in <i>cbd ^KS171</i> mutants.

<p>(<b>A–C</b>) 2^nd instar larval brain. (<b>D–F</b>) early 3^rd instar larval brain. Scale bar in (<b>F</b>) equals 25 µm and applies to (<b>A–F</b>). (<b>G–I</b>) late 3^rd instar larval brain. (<b>J–L</b>) pupal brain 0–2 h APF. (<b>M–O</b>) pupal brain 8–9 h APF. Scale bar in (<b>O</b>) equals 25 µm and applies to (<b>G–O</b>).</p

The <i>cbd</i> mutant phenotype could be significantly rescued when <i>ten-a</i> was driven by <i>C767</i>-Gal4.

<p>(<b>A, B</b>) <i>WTB</i> showed normal FB and EB. (<b>C–F</b>) Both UAS-<i>ten-a</i> and <i>C767</i>-Gal4 in the <i>cbd ^KS171</i> background showed defect in FB and EB. (<b>G, H</b>) FB and EB were restored to normal when UAS-<i>ten-a</i> was driven by <i>C767</i>-Gal4. (<b>I</b>) Percentage of normal FB and EB in controls (5.6% for <i>cbd ^KS171</i>;UAS-<i>ten-a</i>, n = 36; 10% for <i>cbd ^KS171</i>;<i>C767</i>-Gal4/+, n = 30) and in flies with UAS-<i>ten-a</i> driven by <i>C767</i>-Gal4 (36%, n = 25). Two tailed Fisher exact test. *<i>P</i><0.05, **<i>P</i><0.01, ***<i>P</i><0.001. When <i>ten-a</i> over-expressing flies were kept at 18°C, 47% (n = 32) of flies showed a normal FB and EB, much higher than control flies (12.5% for <i>cbd ^KS171</i>;UAS-<i>ten-a</i>, n = 24; 11.1% for <i>cbd ^KS171</i>;<i>C767</i>-Gal4/+, n = 18). Scale bar, 25 µm. <i>Arrows</i> indicate the central complex defect.</p

The expression pattern of <i>C767</i>-Gal4 and DN-cadherin signal during FB formation in wild type flies.

<p>(<b>A–C</b>), The expression pattern of <i>C767</i>-Gal4 (green) and DN-cadherin signal (magenta) in a 2^nd instar larval brain. (<b>D–F</b>) The expression pattern of <i>C767</i>-Gal4 (green) and DN-cadherin signal (magenta) in an early 3^rd instar larval brain. Scale bar in (<b>F</b>) equals 25 µm and applies to (<b>A–F</b>). (<b>G–I</b>) The expression pattern of <i>C767</i>-Gal4 (green) and DN-cadherin signal (magenta) in a late 3^rd instar larval brain. (<b>J–L</b>) The expression pattern of <i>C767</i>-Gal4 (green) and DN-cadherin signal (magenta) in a pupal brain at 0–2 h APF. (<b>M–O</b>) The expression pattern of <i>C767</i>-Gal4 (green) and DN-cadherin signal (magenta) in a pupal brain at 8–9 h APF. Scale bar in (<b>O</b>) equals 25 µm and applies to (<b>G–O</b>).</p

The projection tracts of both F1 neurons and F5 neurons appeared to be normal in <i>cbd ^KS171</i> mutants.

<p>(<b>A–D</b>) Neural projection and arborizations of F1 neurons in wild type flies and <i>cbd ^KS171</i> mutants. (<b>E–H</b>) Neural projection and arborizations of F5 neurons in wild type flies and <i>cbd ^KS171</i> mutants. Scale bar, 25 µm. <i>Arrowheads</i> indicate the normal neural projection.</p

<i>ten-a</i> deficiency line <i>ten-a^#900</i> and down-regulated <i>ten-a</i> expression by RNAi caused FB and EB defects.

<p>(<b>A, B</b>) <i>ten-a^#900</i> showed a FB and EB defect. (<b>C–H</b>) <i>cbd ^KS171</i>, <i>cbd ²²⁵⁴</i> and <i>cbd ^KS96</i> could not complement the FB and EB defect of <i>ten-a^#900</i>. (<b>I–L</b>) Both the FB and the EB were destroyed when <i>ten-a</i> was down-regulated by driving expression of UAS-<i>ten-a</i>^RNAi with <i>tub</i>-Gal4. (<b>M–N</b>) Both the FB and the EB were destroyed when <i>ten-a</i> was down-regulated by driving expression of UAS-<i>ten-a</i>^RNAi with pan-neuronal <i>elav</i>-Gal4. (<b>O–P</b>) Both the FB and the EB were normal when <i>ten-a</i> was down-regulated by driving expression of UAS-<i>ten-a</i>^RNAi with pan-glial <i>repo</i>-Gal4. Scale bar, 25 µm. <i>Arrows</i> indicate the central complex defect.</p

Microstructural mechanisms imparting high strength-ductility synergy in heterogeneous structured as-cast AlCoCrFeNi2.1 eutectic high-entropy alloy

The dual-phase AlCoCrFeNi2.1 eutectic high-entropy alloy (EHEA) presents a promising solution to the strength-ductility trade-off dilemma, making it a highly desirable option for structural materials with vast potential applications. However, the relationship between the mechanical properties and the unique as-cast heterostructures needs to be further revealed. Here, we conducted in-situ tensile experiments of the as-cast EHEA to unveil the mesoscopic/microscopic microstructural mechanisms of strength-ductility synergy via investigating the dynamic real-time plastic deformation behaviors and crystallographic information evolution, as well as characterizing the deformed microstructures via transmission electron microscopy. The results indicate that the sequential dominant heterogeneous deformation induced hardening resulting from the incompatible plastic deformation between different types of heterogeneous microstructures is the primary source of its remarkable strength-ductility synergy. Moreover, the unique elongated lamellar microstructures of the as-cast EHEA offer numerous phase boundaries, and the growth twins in the face-centered cubic (FCC) phase generate abundant twin boundaries, all of which contribute to boundary strengthening and further enhance the strength and ductility of the as-cast EHEA. Furthermore, abundant cross-slip and dislocation substructures in the FCC phase provide strain hardening for as-cast EHEA, while body-centered cubic phase contributes to the high strength through precipitation hardening. Consequently, the heterostructure induced multiple strengthening mechanisms are responsible for the high strength-ductility synergy in the as-cast EHEA. The present work provides a new perspective to explain the strength-ductility synergy of similar heterogeneous structured alloys