Table S1. B. mori genes studied using transposon

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Table S1. B. mori genes studied using transposon-based technologies and genome-editing technologies
Target genes
Type of manipulation
Results/Phenotypes
BmFtz-F1
Inducible expression using Dmhsp70
promoter
Overexpression using Gal4/UAS
system
Overexpression using Gal4/UAS
system
Inducible transgenic RNAi using
Dmhsp70 promoter
Binary transgenic RNAi using
Gal4/UAS system
Overexpression using Gal4/UAS
system
Overexpression using Gal4/UAS
system
Overexpression using Gal4/UAS
system
Overexpression using Gal4/UAS
system
Overexpression using Gal4/UAS
system
Ubiquitous
expression
using
BmNPV ie1 promoter
Ubiquitous
expression
using
BmNPV ie1 promoter
Overexpression using Gal4/UAS
system
Ubiquitous
expression
using
BmActin3 promoter
Overexpression using Gal4/UAS
system
Overexpression using Gal4/UAS
system
Ubiquitous
expression
using
BmNPV ie1 promoter
Expression of BmFtz-F1 in transgenic silkworms was induced at different stages of development and in
diverse tissues after heat shock.
Overexpression of BmCBP in both the midgut and middle silk gland of transgenic silkworms restored the
carotenoid-based yellow phenotype in a colorless hemolymph strain.
Overexpression of BmKIT3R in the pupa stage of transgenic silkworms resulted in the failure of some pupae
to metamorphose into moths.
Expression of BmEH in the whole body of transgenic silkworms was significantly repressed after heat
shock, and caused the hamperness of pupal–adult eclosion and reduction of egg fertility.
Knockdown of ecdysis-triggering hormone gene BmETH with Gal4/UAS RNAi system leads to lethal
ecdysis deficiency in transgenic silkworm.
Overexpression of Bmnsd-2 in the midgut of transgenic silkworms restored virus susceptibility of silkworm
to B. mori densovirus type 2, a parvo-like virus that replicates only in midgut columnar cells.
Overexpression of BmBLOS2 in the whole body of transgenic silkworms partially rescued the translucent
phenotype observed in distinct oily (od) mutants, which is characterized by translucent larval integument.
Overexpression of the wild-type allele of BmCYP15C1 in corpus allatum of transgenic dimolting (mod)
mutants rescued precocious metamorphosis of mod larvae.
Overexpression of BmaaNAT in the whole body of transgenic silkworms changed the color of first-instar
larvae from black to a distinctive light brown color, and lightened adult antenna coloration.
Overexpression of Bmebony in the whole body of transgenic silkworms changed the larval body color of
older instars, and lightened adult antenna coloration.
Expression of female-specific spliced form of Bmdsx (BmdsxF) in the whole body of transgenic males
repressed expression of the pheromone-binding protein gene that is preferentially expressed in males.
Expression of Bmdsx minigene in the whole body of transgenic silkworms resulted in sex-specific
alternative splicing similar with the pattern of endogenous Bmdsx.
Overexpression of BmJHE in the whole body of transgenic silkworms induced premature metamorphosis at
the third-instar larvae.
Expression of BmKMO in the whole body of transgenic silkworms rescued the phenotypic change observed
in the white egg 1 (w-1) mutant, which is characterized by white eyes and white eggs.
Overexpression of BmCameo2 in the middle silk gland of transgenic silkworms restored the accumulation of
lutein in the middle silk gland, and produced yellowish colored cocoons.
Overexpression of BmRas1CA in the posterior silk gland of transgenic silkworms increased cell size and
protein synthesis in the posterior silk gland, and improved silk yield.
Expression of Bmlipase-1 in the whole body of transgenic silkworms enhanced resistance of silkworms to
BmNPV.
BmCBP
BmKIT3R
BmEH
BmETH
Bmnsd-2
BmBLOS2
BmCYP15C1
BmaaNAT
Bmebony
BmdsxF
Bmdsx minigene
BmJHE
BmKMO
BmCameo2
BmRas1CA
Bmlipase-1
References
1
[22]
[28]
[33]
[47]
[48]
[55]
[56]
[87*]
[88*]
[88*]
[89*]
[90*]
[91*]
[92*]
[93*]
[94*]
[95*]
BmSCRB15
BmBLOS2
Overexpression using Gal4/UAS
system
Ubiquitous and ectopic expression
using B. mori ecdysone receptor B1,
BmActin3, and Dmhsp70 promoter
Ubiquitous
expression
using
BmActin4 promoter
Ectopic expression using B. mori
vasa-like promoter
Ectopic expression using BmfibL
promoter
Overexpression using Gal4/UAS
system
Overexpression using Gal4/UAS
system
Overexpression using Gal4/UAS
system
Ubiquitous
expression
using
BmActin3 promoter
Gene knockout using ZFN
Bmwh3
Gene knockout using ZFN
BmfibH
Gene knockout using ZFN
BmBLOS2
Gene knockout using TALEN
Bmre
Gene knockout using TALEN
Bm702
Gene knockout using TALEN
Bmdsx
Gene knockout using TALEN
Bmapontic-like
Gene knockout using TALEN
BmfibH
Gene knockout using TALEN
BmWnt1
BmdsxM
Bmovo-1
BmcecropinB
BmAntp
BmCYP18A1
BmLet-7
Bmapontic-like
Overexpression of BmSCRB15 in the middle silk gland of transgenic silkworms enhanced selective
β-carotene uptake by the middle silk gland, and produced yellowish colored cocoons.
Expression of BmWnt1 in the larval stage of transgenic silkworms caused ectopic pigmentation in the larval
cuticle as observed in normal mutant, multi lunar (L).
[96*]
Expression of male-specific spliced form of Bmdsx (BmdsxF) in the whole body of transgenic females
affected the formation of the chitin plate in females and reduced female copulation.
Expression of Bmovo-1 in the gonad of transgenic silkworms increased oviposition number and elevated the
trehalose contents of hemolymph and ovaries.
Expression of BmcecropinB in the posterior silk gland of transgenic silkworm enhanced the antibacterial
properties of cocoons.
Overexpression of BmAntp in the fifth-instar larvae of transgenic silkworms induced ectopic expression of
ser1 in the posterior silk gland.
Overexpression of BmCYP18A1 in the middle silk gland or in all tissues resulted in developmental
arrestment of transgenic animals during the final instar larval stage.
Overexpression of microRNA BmLet-7 spongeubiquitously decreased expression of BmLet-7, leading to
developmental arrestment during the larvalelarval and larvalepupal transition.
Expression of Bmapontic-like in the larval stage of transgenic silkworms induced additional melanin
pigmentation in the larval epidermis.
Knockout of BmBLOS2 resulted in somatic and germ-line phenotypes similar with the od mutant, which is
characterized by translucent larval integument.
Knockout of Bmwh3 resulted in somatic phenotypes similar with the Bmwh3 mutant, which is characterized
by translucent larval skin and white eggs, but failed to obtain germ-line mutants.
Knockout of BmfibH resulted in germ-line mutants, in which the posterior silk gland was strongly degraded
and negligible amounts of fibroin was detected.
Knockout of BmBLOS2 resulted in somatic and germ-line phenotypes similar with the od mutant, which is
characterized by translucent larval integument.
Knockout of Bmre resulted in somatic and germ-line phenotypes similar with the red egg mutant, which is
characterized by an orange egg color.
Comicroinjection of TALEN pairs for Bm702 (an endogenous gene which is 8.9 Mb downstream BmBLOS2)
and BmBLOS2 induced heritable large chromosomal structure variation.
Knockout of female-specific exon of Bmdsx resulted in somatic mutations and female mutants lost fecundity
because of lack of egg storage.
Knockout of Bmapontic-like caused white patches in the larval epidermis of marking mutants Striped (pS),
which is characterized by solid black larval skin except for the posterior margin of each segment.
Knockout of BmfibH resulted in germ-line mutants, in which the posterior silk gland was strongly degraded
and negligible amounts of fibroin was detected.
[98*]
2
[97*]
[99*]
[100*]
[101*]
[102*]
[103*]
[104*]
[66]
[66]
[68]
[73-75,77,105*]
[75]
[77]
[84]
[104*]
[106*]
BmBLOS2
Gene knockout using CRISPR/Cas9
BmKu70
Gene knockout using CRISPR/Cas9
BmTh
Gene knockout using CRISPR/Cas9
Bmok
Gene knockout using CRISPR/Cas9
BmKMO
Gene knockout using CRISPR/Cas9
Bmtan
Gene knockout using CRISPR/Cas9
Bmre
Gene knockout using CRISPR/Cas9
Bmfl
Gene knockout using CRISPR/Cas9
Bmyellow-e
Gene knockout using CRISPR/Cas9
BmKynu
Gene knockout using CRISPR/Cas9
Bmebony
Gene knockout using CRISPR/Cas9
Knockout of BmBLOS2 resulted in somatic and germ-line phenotypes similar with the od mutant, which is
characterized by translucent larval integument.
Knockout of BmKu70 resulted in germ-line mutants with no significant phenotype, in which the frequency
of homologous recombination mediated targeted gene knockin could be enhanced.
BmTh gene interruption was effectively induced by the CRISPR/Cas9 system in the injected generation
(G0). The phenotype of knockout mutants was not mentioned in the reference.
Knockout of Bmok resulted in somatic and germ-line phenotypes similar with the ok mutant, which is
characterized by a change in the larval cortex from translucent to turbid.
BmKMO gene interruption was effectively induced by the CRISPR/Cas9 system in G0 mosaics. The
phenotype of knockout mutants was not mentioned in the reference.
Bmtan gene interruption was effectively induced by the CRISPR/Cas9 system in G0 mosaics. The phenotype
of knockout mutants was not mentioned in the reference.
Bmre gene interruption was effectively induced by the CRISPR/Cas9 system in G0 mosaics. The phenotype
of knockout mutants was not mentioned in the reference.
Bmfl gene interruption was effectively induced by the CRISPR/Cas9 system in in G0 mosaics. The
phenotype of knockout mutants was not mentioned in the reference.
Bmyellow-e gene interruption was effectively induced by the CRISPR/Cas9 system in G0 mosaics. The
phenotype of knockout mutants was not mentioned in the reference.
BmKynu gene interruption was effectively induced by the CRISPR/Cas9 system in G0 mosaics. The
phenotype of knockout mutants was not mentioned in the reference.
Bmebony gene interruption was effectively induced by the CRISPR/Cas9 system in G0 mosaics. The
phenotype of knockout mutants was not mentioned in the reference.
[81]
[107*]
[108*,109*]
[108*]
[108*]
[108*]
[109*]
[109*]
[109*]
[109*]
[109*]
* These references do not appear in the main document and are listed as following.
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90.
91.
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