Morpholino

MO1-mir9

ID

ZDB-MRPHLNO-081013-4

Name

MO1-mir9

Previous Names

dre-mir-9 MO (1)
MO1-mirn9 (1)

Targets

dre-mir-9-1 (1)
mir9-2 (1)
mir9-3 (1)
mir9-4 (1)
mir9-5 (1)
mir9-6 (1)
mir9-7 (1)

Sequence

5' - TCATACAGCTAGATAACCAAAGA - 3'

Disclaimer

Although ZFIN verifies reagent sequence data, we recommend that you conduct independent sequence analysis before ordering any reagent.

Note

None

Genome Resources

None

Target Location

View all 7 target locations

Genomic Features

No data available

Expression

Gene expression in Wild Types + MO1-mir9

No data available

Phenotype

Phenotype resulting from MO1-mir9

No data available

Phenotype of all Fish created by or utilizing MO1-mir9

Phenotype	Fish	Conditions	Figures
midbrain hindbrain boundary increased length, abnormal	AB + MO1-mir9	standard conditions	Fig. 6 from Leucht et al., 2008
midbrain hindbrain boundary increased width, abnormal	AB + MO1-mir9	standard conditions	Fig. 6 from Leucht et al., 2008
telencephalon ventricular zone her4.1 expression decreased amount, abnormal	AB + MO1-mir9	control	Fig. 3 from Katz et al., 2016
neuron differentiation disrupted, abnormal	AB + MO1-mir9	standard conditions	Fig. 7 from Leucht et al., 2008
brain onecut2 expression increased amount, abnormal	WT + MO1-mir9	standard conditions	Fig. S4 from Madelaine et al., 2017
hindbrain lateral region has extra parts of type neuron, abnormal	WT + MO1-mir9	standard conditions	Fig. 3 from Coolen et al., 2012
brain onecutl expression increased amount, abnormal	WT + MO1-mir9	standard conditions	Fig. S4 from Madelaine et al., 2017
retina nr2e1 expression increased amount, abnormal	WT + MO1-mir9	standard conditions	Fig. S4 from Madelaine et al., 2017
brain vegfaa expression increased amount, abnormal	WT + MO1-mir9	standard conditions	Fig. 2 , Fig. 3 from Madelaine et al., 2017
hindbrain exit from mitosis delayed, abnormal	WT + MO1-mir9	standard conditions	Fig. 3 from Coolen et al., 2012
hindbrain cell proliferation in hindbrain ventricular zone increased occurrence, abnormal	WT + MO1-mir9	standard conditions	Fig. 2 from Coolen et al., 2012
retina onecut1 expression increased amount, abnormal	WT + MO1-mir9	standard conditions	Fig. S4 from Madelaine et al., 2017
brain onecut1 expression increased amount, abnormal	WT + MO1-mir9	standard conditions	Fig. S4 from Madelaine et al., 2017
retina vegfaa expression increased amount, abnormal	WT + MO1-mir9	standard conditions	Fig. 2 from Madelaine et al., 2017
hindbrain neurogenesis increased occurrence, abnormal	WT + MO1-mir9	standard conditions	Fig. 3 from Coolen et al., 2012
retina onecut2 expression increased amount, abnormal	WT + MO1-mir9	standard conditions	Fig. S4 from Madelaine et al., 2017
retina onecutl expression increased amount, abnormal	WT + MO1-mir9	standard conditions	Fig. S4 from Madelaine et al., 2017
hindbrain neurogenesis increased duration, abnormal	WT + MO1-mir9	standard conditions	Fig. 3 from Coolen et al., 2012
brain nr2e1 expression increased amount, abnormal	WT + MO1-mir9	standard conditions	Fig. S4 from Madelaine et al., 2017
brain vegfaa expression amount, ameliorated	WT + MO1-mir9 + MO1-nr2e1 + MO1-onecutl	standard conditions	Fig. 3 from Madelaine et al., 2017
hindbrain lateral region has extra parts of type neuron, abnormal	knu3Tg + MO1-mir9	standard conditions	Fig. 3 from Coolen et al., 2012
hindbrain neurogenesis increased occurrence, abnormal	knu3Tg + MO1-mir9	standard conditions	Fig. 3 from Coolen et al., 2012
primordial hindbrain channel increased thickness, abnormal	la116Tg + MO1-mir9	standard conditions	Fig. 2 from Madelaine et al., 2017
central artery vascular sprouts increased amount, abnormal	la116Tg + MO1-mir9	standard conditions	Fig. 2 from Madelaine et al., 2017
primordial hindbrain channel endothelial cell increased amount, abnormal	la116Tg + MO1-mir9	standard conditions	Fig. 2 from Madelaine et al., 2017
dorsal telencephalon neuronal stem cell division increased occurrence, abnormal	mi2001Tg + MO1-mir9	standard conditions	Fig. 2 from Katz et al., 2016
dorsal telencephalon stem cell proliferation increased occurrence, abnormal	mi2001Tg + MO1-mir9	standard conditions	Fig. 2 from Katz et al., 2016
radial glial cell nucleus Ab1-ago labeling decreased amount, abnormal	mi2001Tg + MO1-mir9	control	Fig. 4 from Katz et al., 2016
primordial hindbrain channel increased thickness, abnormal	s896Tg + MO1-mir9	control	Fig. 2 from Madelaine et al., 2017
central artery vascular sprouts disorganized, abnormal	s896Tg + MO1-mir9	control	Fig. 2 from Madelaine et al., 2017
central artery vascular sprouts decreased amount, abnormal	s896Tg + MO1-mir9	control	Fig. 2 from Madelaine et al., 2017
central artery decreased thickness, abnormal	s896Tg + MO1-mir9	control	Fig. 2 from Madelaine et al., 2017
middle mesencephalic central artery malformed, abnormal	s896Tg + MO1-mir9	control	Fig. 2 from Madelaine et al., 2017
hindbrain blood vessel malformed, abnormal	s896Tg + MO1-mir9	control	Fig. 2 from Madelaine et al., 2017
central artery vascular sprouts amount, ameliorated	s896Tg + MO1-mir9	chemical treatment by environment: semaxanib	Fig. 2 from Madelaine et al., 2017
retina blood vessel decreased amount, abnormal	s896Tg + MO1-mir9	standard conditions	Fig. 6 from Madelaine et al., 2018
hyaloid vessel malformed, abnormal	s896Tg + MO1-mir9	standard conditions	Fig. 6 from Madelaine et al., 2018
brain blood vessel malformed, abnormal	s896Tg + MO1-mir9	control	Fig. 2 from Madelaine et al., 2017
central artery disorganized, abnormal	s896Tg + MO1-mir9	control	Fig. 2 from Madelaine et al., 2017
retina blood vessel malformed, abnormal	s896Tg + MO1-mir9	control	Fig. 2 from Madelaine et al., 2017

Citations