The Mutant of Mulberry Silkworm

The silkworm produces various types that are different from the standard type in terms of body shape, color, morphology, and physiological and biochemical characteristics during each period from egg to adult, and its individuals are called mutants. From silkworm eggs to adults, more than 400 mutants of various types have been discovered, distributed in various linkage groups. The main types are as follows:

1. Egg

Oval

The oval shape is determined by the mother’s body. The standard ovoid shape is a short ellipse with a slightly pointed end with a fine hole. Mutant types of egg shells include large egg (Ge, 1-14.0) (in parentheses, the gene symbol, the linkage group and its locus, the same below), elliptic egg (elp, 18-9.9), kidney-shaped egg (ki, 6-8.6), small eggs (sm, 3-41.8), spindle eggs (sp, 23-28.7), etc., all have pseudomaternal inheritance.

Eggshell

The standard egg shell is colorless and translucent, and the mutant type can be colored and opaque. Such as green egg shell (Gre, 1-46.4), white edged egg (Se, 15-16.9), spotted gray egg (mgr, 6-8.9), and the gray egg mutant Gr allele at the second chromosome 6.9 locus group.

Egg color

The egg color is mainly determined by the color of the serosa. The standard type is dark brown, and the formation of serosal pigments needs to go through the process of tryptophan→formylkynurenine→kynurenine→3-hydroxykynurenine→pigment. If any of these steps are caused by mutations Obstructed, that is, the brown pigment cannot be formed, and the mutant type of egg color is produced, which makes the egg color white, rust, cocoa, peach, red, brown, etc. The inheritance of egg color is common inheritance. Among them, the pink-eye white egg (pe, 5-0.0) and red egg (re, 5-31.7) are important egg color marker genes, which are widely used in specific locus methods and become important research materials for silkworm mutations.

2. Larva

The standard type is dark brown, and the mutants include red silkworms (ch, 13-9.6), dominant red silkworms (I-a, 9-5.9) and sex-linked red silkworms (sch, 1-21.5). The body color of red silkworm is russet, even in the silkworm stage, the markings and colored areas of the valve sieve plate are also shown as russet. When combined with dark spots (p ^M ) or black spots (p ^S ), the markings are also auburn. But the black of p ^M and the brown of p ^S are not affected by sex-linked red ants.

Brindle

The markings are mainly determined by the nature and distribution of pigments in dermal cells and epithelial cells. The common spot (+ ^P , or p ³ ) is usually regarded as the standard type of silkworm, while the prime silkworm (p) is regarded as the most basic mutant type. Marking is the most studied trait in the morphological inheritance of silkworm, so the mutations found are also extremely abundant. Locus 0.0 on the second chromosome is a p-multiple allele group, and more than 15 mutants have been found. Their obvious and hidden relationship is black silkworm>black silkworm≥dark silkworm> coal gray silkworm> common silkworm> plain silkworm (pB>p ^S ≥p ^M >p ^Sa >+ ^P >p). After some speckle genes, such as ps and Ze, are transposed on the W chromosome, the restricted speckles produced can be directly used in production. There are many mutant types of markings, the more common ones are brown round spots (L, 4-15.3), tabby (Ze, 3-20.8), quail spots (q, 7-0.0), and multiple star patterns (ms, 12-5.5) Wait.

Body color and oiliness

Normal silkworm dermal cells contain a lot of white urate crystals, so the skin is white and opaque. The urate content of the mutant dermal cells of the oily silkworm is about 3 to 80% of that of the normal silkworm, resulting in different degrees and different forms of oily silkworms. Oily silkworm sex is not only manifested in the skin, but also in the serosal membranes and tissues and organs formed by the ectoderm. Some oil silkworm mutants have varying degrees of lethality and sterility. It is known that there are more than 35 genes on different loci of different chromosomes that can produce oil silkworms. Except for the dominant short-section oil silkworm and the dominant Chikuzi oil silkworm, they are all recessive. The mutant type of luteal color (lem, 3-0.0) has a large amount of 7.8-dihydropterin (mepterin) in its dermal cells, and its body color is lemon yellow. On the contrary, its suppressor gene luteal color suppression (i-lem2-29.5) makes the body color extremely light. Red ripe (R _s ) is another mutant type, and the skin of ripe silkworm is dark red.

Body shape

The most famous body shape mutant is Longjiao (K, 11-23.2), which has a pair of tumor-like protrusions on the back of the second, third, fifth, and eighth links, which can be identified in the pupal stage. When coexisting with brown round spot (L), brown round spot tumor is formed. However , when coexisting with black silk (p ^s ), the tumor becomes significantly smaller due to the inhibition of p ^s . In addition, there are long-knot silkworms with 1, 2 abdominal segments longer than normal silkworms (e, 1-36.4); larvae have narrow chests and a spindle-shaped narrow breasts (nb, 19～0.0) with enlarged abdomen; inner edges of each link are raised The slub-shaped stone silkworm (st, 8-0.0) and other body shape mutants.

color

The blood color of the standard type is light yellow or colorless. In most cases, the blood color is the same as the cocoon color. The yellow blood mutant (Y, 2-25.6) is dark yellow due to the large amount of carotenoids in the blood, and its cocoons are also yellow cocoons. But its inhibitory genes yellow blood inhibitor (1,9-0.0) and coalin yellow blood inhibitor (Is, 9-0.0) can inhibit the expression of Y and form white cocoons. For example, most European white cocoon species become dominant white cocoon species. Another mutant type is red blood (rb, 21-0.0), homozygous (rb/rb) blood does not turn into normal black when exposed to the air, but slightly red.

3. Cocoon

Cocoon color

Generally, white cocoons are regarded as standard. The mutant cocoon colors include yellow cocoons formed by carotenoids, carotene and lutein, and green cocoons formed by flavonoid pigments. But the former pigment is only distributed in sericin, while the latter is distributed in sericin and fibroin. The outer layer of golden cocoon (C) is golden and the inner layer is almost white; the inner layer of yellow cocoon (C ⁱ ) is yellow but the outer layer is very lightly colored; the inner and outer layers of straw-colored cocoon (C ^st ) are both light yellow. The three constitute a multiple allele series (12-7.2), all of which require the presence of yellow blood (Y). The expression of flesh-colored cocoons (F, 6-13.6) must coexist with Y and C. There are three types of green cocoon genes: green cocoon a (Ga), green cocoon b (Gb, 7-7.0) and green cocoon c (Gc, 15-?). When Gc and Gb coexist, a light green cocoon is formed. Gc has an epistatic effect on Ga, and Gc is inherited independently. In addition, there are mutants such as rusty cocoons (Rc, 2-31.8), yellow fluorescent cocoons (Yf), yellow-brown cocoons (Yr, 6-18.7) and wild silkworm yellow cocoons (Ymc).

Cocoon shape and layer

In general, the cocoons of Chinese species are mostly oval, Japanese species are mostly corrugated, European species are mostly oblong with shallow corsets, and tropical local species are mostly fusiform, with denser cocoon layers and shrinkage.

4. Pupa

The standard type is yellowish-brown, oval, with wing buds on the chest, covering the ventral surface of the second abdominal segment, and the pupa-colored mutants include black pupa (bp, 11-40.3) and white wing pupa (Wp). Wing mutants include crawfish pupae (cf, 13-20.9), crawfish pupae cf-e: 4-0.0, and crawfish pupae (cf-e: 4-0.0). The wing buds of crawfish pupae protrude beyond Outside the pupa. Winged pupa (Cw, 13-) and wingless pupa (fl, 10-13.0) and so on. Wing-shaped mutations are often not conducive to pupation and mating.

5. Moth

The body and wings of the standard moth are covered with scales. The scales are white except in spots and markings. The wings are approximately fan-shaped. The morphological mutations of silkworm moths are mostly manifested in body color, compound eye color and wing morphology. The mutants of moth body color include black moth (Bm, 17-0.0), wild silkworm black moth (Wm), white belt black wings (wb, 5-35.0), wild silkworm wing spots (Ws, 17-14.7) and yellow antennae (ya )Wait. A larval striped mutant darkened (mln) moth is also black. Wing-shaped mutants include small wing (mp, 11-51.8), young wing (mw, 22-16.3), degenerative radial vein (rv), sex-linked wingless (rw.1-22.8), short wing (Swi) , Trace wings (Vg, l-38.7) and wrinkled wings (wri, 14-0.0) and so on. The mutant types of compound eyes include glossy ommatidium (ve, 6-11.1) and glossy eye (lu, 16-0.0).

6. Physiological and biochemical mutants

Chemistry

It is generally believed that duality is a standard type. The genetic inheritance includes maternal inheritance and general inheritance. The mutant type that determines maternal inheritance has a series of sex-associated Hs alleles, but it is also modified by a series of autosomal genes H ₁ h ₁ H ₂ h ₂ and H ₃ h ₃ . The V allele (6-21.5) on chromosome 6 is decisive, but it is largely affected by the sexual maturation genes Lm and Lme (1-2.0). The dominant-recessive relationship of the V allele is: V ¹ >+ ^v >V ³ . The chemical mutants that determine general inheritance include colored non-dormant eggs (pnd, 11-53.7) and dead eggs (1-n, 12-21.0) and so on.

Sleepiness

4 sleep is considered to be the standard type (+M). The silkworm has at least 5 different dormancy properties of 2, 3, 4, 5 and 6 dormancy. The main mutants that determine dormancy are M alleles (6-3.0). M ² , M ³ and M ⁵ determine the second, third and fifth dormancy, respectively, and the dominant-recessive relationship is M3>+M>M5. But its performance is partially affected by the mature genes Lm and Lme. In addition, there are also mutants such as 2 sleep (mod, 11-11.6), recessive 3 sleep (rt, 7-9.0), and delayed sleep onset (rm, 3-6.5).

feeding habits

The standard type feeds on mulberry leaves. Some mutants of feeding habits prevent silkworms from distinguishing mulberry leaves from other leaves. If eating habits are abnormal (Np, 11-30.5), beet leaves can be eaten. Yokoyama’s sawa-J system can eat cabbage leaves and some fruits. According to research, the strong adaptability that is fully adapted to eating artificial feed is simple and dominant to the weak adaptability that can hardly grow.

Abnormal development and differentiation

The abnormalities of somites and appendages are the E-quasi-allele group in the 0.0-1.4 region of chromosome 6. All are related to the appearance of excess feet and excess markings, as well as the abnormalities of the gonads and reproductive organs, which also play a role in the differentiation of somites during embryonic development. Most of these genes have a recessive lethal effect when they are homozygous, and they are an important tool for the study of developmental genetics. This group includes silkworm excess foot (E), excess half moon pattern (E ^Ca ), gonad abnormality (E ^Gd ), Kp excess foot (E ^Kp ), excess foot without half moon pattern (E ^Nc ) and triple half moon pattern (E ^Tc ) There are 31 mutants in total. In addition, there is a similar gene without streaking (Nc, 6-1.4). Some mutants related to abnormal differentiation of somites and appendages, including malformation (mal, 4-30.1), burnt silkworm (Bu, 11-28.7), excess valve (es, 12-4.3), genetic mosaic (mo ), body segment deformity (mse), footless (ap, 3-22.3), fifth body segment excess foot (sl-V, 21-19.4) and so on.

Slow growth silkworm (Rt, 2-), γ-ray-induced growth retardation (Rg, 3-24.9), slow growth (Slg, 15-), Tsujita dwarf silkworm (Df-t, 20-11.0) and K- Mutants such as the dwarf silkworm (dw-k10-0.0) affect the normal growth and development of the silkworm, and the silkworm body is thin.

In males, the mutants that cause infertility include penile muscle degeneration (slp), abnormal fine clip (sls), and lack of sperm. In terms of females, in addition to the infertility caused by some E-group genes, there are also tightening of the vagina (cv and cd) and so on.

7. Enzymes

The method of gel electrophoresis was used to study the various enzymes of silkworm, and numerous biochemical genetic mutations have been discovered. In terms of amylase, mutants with weak digestive juice amylase activity (ae, 8-2.8) and body fluid amylase activity (be, 8-4.2) were found. In terms of phosphatase, according to the migration speed of isoenzymes in electrophoresis, it was found that the midgut alkaline phosphatase has two mutant types, Aph ₁ and Aph ₂ , and the blood acid phosphatase type (23-) has BphA, BphB, BphC, BphD, and BphD. There are 5 mutant types of BphO (deficient). In terms of lipase, blood lipase types include Bes ^A, Bes ^B , Bes ^C, and Bes ^D (11-33.9), and body sebum lipase types are: Ies ^A , Ies ^B , Les ^C , Ies ^AB , Ies ^AC and Ies ^O ; egg lipases include Ees ₁ , Ees ₂ , Ees ₃ , Ees _4, and Ees ₅ ; silk gland lipases include Ses ^A , Ses ^B , and Ses ^OAnd other mutants. In addition, there are blood tyrosinase (tr) mutants that have low blood tyrosinase activity from larvae to pupal stage, and chymotrypsin inhibitor (Ict) that inhibits chymotrypsin activity.

Protein and blood cells

Using gel electrophoresis, a series of non-enzymatic protein mutants were discovered.

1. Alb-allele (19-6.2). Including fast-migrating blood albumin F (Alb ^F ) and slow-migrating blood albumin S (Alb ^s ) are a pair of equal dominant genes.
2. pt-3 allele (14-), a blood protein that expresses the solubility of albumin and migration to the Alb region, including fast-migrating Pt ^F s and slow-migrating Pt ^S ₃ .
3. Lp alleles (20-6.2), the fast, medium and slow migration of pupal blood lipoproteins in electrophoresis are controlled by the three genes of Lp ^F , Lp ^M and Lp ^S , respectively .
4. Fib-H allele (25-), the migration speed of fibroin heavy chain to the cathode during electrophoresis is controlled by Fib-H ^F , Fib-H ^M and Fib-HS three genes.
5. Light chain fibroin (Fib-L14-). ⑥ No mucus (Ng, 12-21.8). This mutant type has almost no mucus protein formation due to the decrease in the amount of rRNA, and the eggs are only slightly glued.

There are two types of blood cell mutants: dominant globular cell deficiency (Sph, 21-8.4) and recessive globular cell deficiency (Spr, 10-12.1).

8. Lethal

Lethal mutants appear frequently in silkworms, E-group genes, non-half-moon pattern (Nl) and oil silkworms all have varying degrees of lethal effects or homozygous lethality. Most of the lethal effects occur in the embryonic stage, and some occur in the late embryonic stage. There are more than 20 lethal mutants in the embryonic stage, most of which are related to abnormal embryonic development, incomplete differentiation of tissues and organs, and changes in serosal pigments. This type of lethality includes brown dead eggs (1-br, 9-18.1), k lethal eggs (1-k, 6-17.7), birth dead eggs (1-n), lethal spindle eggs (1-sp, 12-) , Leukoplakia dead eggs (1-w, 4-28.4), lethal white eggs (peL, 5-0.0), etc. Mortality in the late embryonic stage is mostly related to hormone system defects, metabolic system disorders, and body shape and skin abnormalities. For example, dominant dwarf silkworm (Df) and k dwarf silkworm (dwk, 10-0.0) are caused by abnormal hormone secretion. Albinism (al, 5-37.9) is fatal due to incomplete differentiation of the body skin and inability to harden. Luteal color is fatal (lem ¹ , 3-0.0), because the skin contains too much mepterin, the skin becomes yellow after peeling, and it is fatal if it cannot eat mulberry. The stinky silkworm (sku, 22-7.1) produces odorous substances due to amino acid metabolism and is fatal. Sleepless silkworms (nm, 11-11.6) die without molting two weeks after hatching, which is related to the abnormality of crimson cells.