FlyBase Allele Report: Dmel\sesB[1]

sesB¹ mutant flies show developmental retardation, epileptic seizures upon mechanical stress (bang sensitivity), hearing impairment, defective male courtship and greatly reduced lifespan. The muscle mitochondrial network in young adult flies appears intact.

Ovary size in sesB¹ mutants is decreased. The mutant females eventually produce eggs in normal, or near normal numbers. Eggs laid by the mutants develop only as far as the late embryo stage, with a tiny number of survivors reaching adulthood (approximately 0.1% of the number of progeny from control crosses). Males are fertile, but show defects in courtship assays.

The developmental delay and seizures can be partially alleviated by transferring the sesB¹ mutation to a mitochondrial DNA background (BER-1) that is thought to increase mitochondrial biogenesis.

(Vartiainen et al., 2014)

Mutant neuroblasts have normal mitochondrial distribution, but the mitochondria are consistently small and spherical throughout the cell cycle compared to wild type.

(Sen et al., 2013)

sesB¹ mutants are developmentally delayed, bang sensitive, display female sterility, and have a short lifespan. The short lifespan phenotype is highly dependent on cytoplasmic background.

(Chen et al., 2012)

In sesB¹ mutants the pronounced apical and basal polarization of the mitochondria in the Malpighian tubules is lost, and they are distributed uniformly throughout the cytoplasm. In particular, the normally prominent threadlike brush border is reduced and its mitochondrial density lower.

sesB¹ mutants display a significantly reduced rate in fluid transport in the Malpighian tubules.

Male viable sesB¹ mutants display a significantly reduced survival compared to controls.

(Terhzaz et al., 2010)

sesB¹ mutants exhibit a significant reduction in lifespan compared to wild-type controls, with a median lifespan of 25 days compared to 50 days.

sesB¹ mutants exhibit some evidence of thoracic ganglion age-dependent neurodegeneration. However, they exhibit only minimal evidence of myopathology by day 10 in the dorsal flight muscles.

sesB¹ mutants have reduced locomotor function and conditional paralysis brought on by mechanical stress.

sesB¹ mutants exhibit a markedly progressive paralysis phenotype brought on by mechanical stress. Young mutants, day 2 and 4, are not more affected by mechanical stress than wild-type, although there is greater variability in recovery time in the mutants than age-matched wild-type animals. However, by day 6, sesB¹ mutants demonstrate significant locomotor impairment. This trend continues as the mutants age, with paralysis typically lasting around 3 minutes by day 24.

(Celotto et al., 2006)

The giant fiber(GF)-dorsal longitudinal indirect flight muscle (DLM) neuronal circuit is more sensitive to seizure induction in mutants than in wild-type flies; seizures can be induced with high-frequency brain stimulation of shorter or less intensity in the mutant animals. The mutant animals show type I seizures.

(Fergestad et al., 2006)

The number of mitochondria in the photoreceptor axons at the level of the lamina is normal in heterozygous flies.

(Chang and Min, 2005)

Homozygous sesB¹ mutants exhibit complete paralysis for >5 seconds after mechanical stress (10s vortex), after which animals slowly right themselves. Once sesB¹ mutants achieve a standing position they are markedly sluggish for 1 to 3 minutes, grooming infrequently.

sesB¹ hetero- and homozygotes do not exhibit any stress-sensitivity when exposed to heat shock.

sesB¹ mutant larvae exhibit a significant decrease in mitochondria at the presynaptic terminal.

In sesB¹ mutants, the neuromuscular junction displays a twofold increase in bouton number.

Evoked synaptic transmission and synaptic current amplitude is not significantly different in sesB¹ mutants compared to controls. mEJC frequency in sesB¹ mutants is similar controls. The average mEJC amplitudes in sesB¹ mutants is not significantly different from controls, indicating normal postsynaptic responses to individual quanta. The distribution of mEJC amplitudes is unaltered. Elevation of "["Ca[2+]"]" to 2.0mM does not alter mEJC frequency and amplitude in sesB¹ mutants, compared to inducing an increase as in controls.

sesB¹ mutants show severe synaptic transmission fatigue, with EJC amplitudes reduced from over 200 nA before high-frequency stimulation onset, to under 10nA after 2mins of stimulation.

sesB¹ neurotransmission shows slow recovery from high-frequency stimulation-induced fatigue and remains significantly attenuated for at least the first minute of recovery.

During high-frequency electrotonic stimulation, sesB¹ EJC amplitudes are significantly attenuated.

Using physiological extracellular "["Ca[2+]"]" (2.0mM), mEJC frequency is reduced in sesB¹ mutants. sesB¹ mutant synapses display no "["Ca[2+]"]" dependence of mEJC frequency.

Between 0.2 and 2.0mM "["Ca[2+]"]", mEJC frequency is unchanged in sesB¹ mutants.

sesB¹ mutants are insensitive to activity-dependent mEJC amplitude modulation.

Pre-synaptic vesicle endocytosis/exocytosis cycling is significantly impaired in sesB¹ mutants.

(Trotta et al., 2004)

90% of the expected number of sesB¹/sesB^org flies survive to adulthood.

(Rikhy et al., 2003)

Flies survive 12 hours of sleep deprivation and show activity patterns during deprivation similar to those of wild-type flies.

(Shaw et al., 2002)

Mutant flies are generally rather hypoactive and have delayed development. After "vortexing" for 10 seconds, 1-2 day old adult hemizygous males are paralysed for 38 +/- 51 seconds, 6 day old males are paralysed for more than 100 seconds and 6 day old homozygous females are paralysed for 71 +/- 53 seconds. Hemizygous males are viable, homozygous females show reduced viability.

(Zhang et al., 1999)

Semilethal: viability at 18^oC and 29^oC is 0--2%, at 25^oC 10%.

(Zhimulev et al., 1987)

Causes adults to be extremely sensitive to mechanical shock (FBrf0030192); paralysis lasts many seconds and recovery is slow; the mutant is also generally inactive and uncoordinated; when stimulated to jump and fly, does so abnormally for short distances; when reared at 29^oC, after being raised at 22^oC.

External Data

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Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

sesB¹ has short lived phenotype, enhanceable by mt:ATPase6¹

(Celotto et al., 2006)

sesB¹ has abnormal locomotor behavior phenotype, enhanceable by mt:ATPase6¹

(Celotto et al., 2006)

sesB¹ has abnormal neuroanatomy phenotype, enhanceable by mt:ATPase6¹

(Celotto et al., 2006)

sesB¹ has paralytic | conditional phenotype, enhanceable by shi[+]/shi¹

(Trotta et al., 2004)

Suppressed by

Statement

Reference

sesB¹ has bang sensitive phenotype, suppressible | partially by srl^+t8.7

(Vartiainen et al., 2014)

sesB¹ has partially lethal - majority die phenotype, suppressible | partially by Cint\AOX^UAS.cFa/Scer\GAL4^da.G32

(Vartiainen et al., 2014)

sesB¹ has majority die during embryonic stage phenotype, suppressible | partially by Cint\AOX^UAS.cFa/Scer\GAL4^da.G32

(Vartiainen et al., 2014)

sesB¹ has paralytic | conditional phenotype, suppressible | partially by Atpα²²⁰⁶/Atpalpha[+]

(Trotta et al., 2004)

sesB¹ has paralytic | conditional phenotype, suppressible by para^ts1

(Trotta et al., 2004)

NOT suppressed by

Statement

Reference

sesB¹ has abnormal developmental rate phenotype, non-suppressible by srl^+t8.7

(Vartiainen et al., 2014)

sesB¹ has partially lethal - majority die phenotype, non-suppressible by Scer\NDI1^UAS.cUa/Scer\GAL4^da.G32

(Vartiainen et al., 2014)

sesB¹ has majority die during embryonic stage phenotype, non-suppressible by Scer\NDI1^UAS.cUa/Scer\GAL4^da.G32

(Vartiainen et al., 2014)

Enhancer of

Statement

Reference

sesB¹ is an enhancer of short lived phenotype of mt:ATPase6¹

(Celotto et al., 2006)

sesB¹ is an enhancer of abnormal locomotor behavior phenotype of mt:ATPase6¹

(Celotto et al., 2006)

sesB¹ is an enhancer of abnormal neuroanatomy phenotype of mt:ATPase6¹

(Celotto et al., 2006)

NOT Enhancer of

Statement

Reference

sesB¹ is a non-enhancer of paralytic | heat sensitive phenotype of shi^BS1

(Rikhy et al., 2003)

sesB¹ is a non-enhancer of paralytic | heat sensitive phenotype of shi²

(Rikhy et al., 2003)

Suppressor of

Statement

Reference

sesB¹/sesB[+] is a suppressor of paralytic | conditional phenotype of Atpα²²⁰⁶

(Trotta et al., 2004)

NOT Suppressor of

Statement

Reference

sesB¹ is a non-suppressor of paralytic | heat sensitive phenotype of shi²

(Rikhy et al., 2003)

sesB¹ is a non-suppressor of paralytic | heat sensitive phenotype of shi^BS1

(Rikhy et al., 2003)

Other

Statement

Reference

sesB¹/sesB[+], sra¹ has bang sensitive phenotype

(Chang and Min, 2005)

Phenotype Manifest In

Enhanced by

Statement

Reference

sesB¹ has adult ventral nerve cord phenotype, enhanceable by mt:ATPase6¹

(Celotto et al., 2006)

Additional Comments

Genetic Interactions

Statement

Reference

Despite an apparent rescue of bang sensitivity of sesB¹, there is no rescue of developmental delay by srl^+t8.7.

(Vartiainen et al., 2014)

The lifespan of sesB¹; mt:ATPase6¹ double mutants reveals an additional impairment of adult viability beyond each of the individual mitochondrial mutants. It is important to note that mt:ATPase6¹ does not appear to compensate for the sesB¹ mutation and improve viability.

Severe neuropathology is observed in aged sesB¹; mt:ATPase6¹ double mutant brains, namely individual large vacuolar structures that are not observed in age-matched animals. Young animals are free of pathology, demonstrating that the neurodegeneration is strictly progressive.

The mt:ATPase6¹ mutant accelerates the sesB¹ degeneration of the thoracic ganglion.

sesB¹; mt:ATPase6¹ double mutants reveal enhanced locomotor impairment with an earlier onset than either of the separate mitochondrial mutants.

(Celotto et al., 2006)

sesB¹/+ ; sra¹ flies are bang sensitive, remaining paralysed for a prolonged period after mechanical stress.

(Chang and Min, 2005)

sesB¹/Atpα²²⁰⁶ mutants exhibit a weaker stress-sensitive paralysis than either homozygous mutant alone, taking 3.6 seconds to achieve a standing position after stress.

sesB¹/para^ts1 double mutants display no significant paralysis after heat shock (90s, 30[o]C) and vortexing (10s).

Heterozygous sesB¹; shi¹ mutants exhibit significantly greater paralysis time after heat shock (90s, 30[o]C) and vortexing (10s) compared to controls.

(Trotta et al., 2004)

Xenogenetic Interactions

Statement

Reference

Expression of Scer\GAL4^da.G32>Zzzz\AOX^Scer\UAS.cFa restores the progeny in sesB¹ females to 15-20% of control crosses. The short lifespan of sesB¹ flies is marginally improved by Zzzz\AOX^Scer\UAS.cFa expression. Zzzz\AOX^Scer\UAS.cFa-expressing males show a statistically significant increase in their lifespan or 3-4 days compared with that of controls, but the effect in females is negligible.

Expression of Scer\GAL4^da.G32>Scer\NDI1^Scer\UAS.cUa fails to restore progeny in sesB¹ females.

(Vartiainen et al., 2014)

Complementation and Rescue Data

Rescued by

sesB¹ is rescued by sesB^+t10.3

(Zhang et al., 1999)

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

93884

sesB¹/FM7a

Notes on Origin

Discoverer

Homyk.

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (4)

Reported As

Symbol Synonym

ANT1

(Celotto et al., 2006)

sesB1

(Zhimulev et al., 1987)

sesB¹

(Fogle et al., 2016, Vartiainen et al., 2014, Sen et al., 2013, Chen et al., 2012, Terhzaz et al., 2010, Toivonen et al., 2007, Celotto et al., 2006, Fergestad et al., 2006, Chang and Min, 2005, Trotta et al., 2004)

Name Synonyms

stress-sensitive B1

(Vartiainen et al., 2014)

Secondary FlyBase IDs

References (18)

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